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Review Article | DOI: https://doi.org/10.31579/IJBR-2021/034
Department of Microbiology, R.D. Gardi Medical College, Ujjain, MP 456001, India
*Corresponding Author: Mahendra K. Bhopale, Ph.D., D.Sc, Director (Research), R.D. Gardi Medical College, Ujjain, MP 456001, India
Citation: Mahendra K. Bhopale (2021) Aspects of Cytokine Response to HIV-1 and Tuberculosis Co-Infection International J. of Biomed Research. 1(8); DOI: 10.31579/IJBR-2021/034
Copyright: © 2021, Mahendra K. Bhopale, This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received: 03 August 2021 | Accepted: 23 August 2021 | Published: 19 November 2021
Keywords: cytokine, HIV-1; tuberculosis; co-infection; immune mechanism
It has been known that HIV-1 infection alters the course of Mycobacterium tuberculosis infection and substantially increases the risk of active tuberculosis (TB). Various cytokines play different roles in HIV-1 and TB individually and in a co-infection stage of disease. IL-2 play CD4+ proliferation, IL-4 activate B cells, CD4 cell IL-6/IL-10 dysregulate and CD4+ T (Th17) cell subset lost during HIV-1 infection. IL-22 and IL-27-producing CD4 (+) T cells play immune reconstitution inflammatory syndrome (IRIS) following the commencement of antiretroviral therapy (ART). Higher values of IFN-γ, IL-2, IL-6 and IL-10 were observed in HIV-positive during anti-tuberculous treatment. Combination antiretroviral therapy in tuberculosis (TB) and HIV-1 infection is associated with an immune reconstitution inflammatory syndrome (TB-IRIS). Based on different roles of each cytokine in HIV-1 and TB individually and co-infection, changes occur in therapy is described in the present review.
TB: Tuberculosis;
TB: Tuberculosis;
TPE: Tuberculous pleural effusion;
TB-IRIS: TB-associated immune reconstitution inflammatory syndrome IRIS: immune reconstitution inflammatory syndrome;
MTB: Mycobacterium tuberculosis;
HIV-1: human immunodeficiency virus type 1;
DC-SIGN: Dendritic Cell-Specific Intercellular adhesion molecule-3- Grabbing Non-integrin;
ART: antiretroviral therapy;
HAART: Highly active antiretroviral therapy;
JAK/STAT: Janus kinase/signal transducers and activators of transcription;
PAMPs: pathogen-associated molecular patterns;
HLA-DR: Human Leukocyte Antigen–DR isotype;
AIDS: Acquired immunodeficiency syndrome;
NKT: Natural killer T cells;
PBMC: peripheral blood mononuclear cell;
LTB: Latent tuberculosis;
MDR-TB: Multidrug-resistant tuberculosis;
MDSC: Myeloid-derived suppressor cells;
EFV: Efavirenz;
RAL: Raltegravir;
7-oxoDHEA: 7-oxodehydroepiandrosterone;
NRTIs: Nucleoside reverse transcriptase inhibitors;
TLR: Toll-like receptor;
RNAi: RNA interference;
MYD88: Myeloid differentiation primary response 88;
IRAK1: Interleukin-1 receptor-associated kinase 1;
NRTIs: Nucleoside reverse transcriptase inhibitors;
NNRTIs: Non-nucleoside Reverse Transcriptase Inhibitors;
TRAF6: Tumor necrosis factor receptor-associated factor 6;
TREM-1: Triggering receptor expressed on myeloid cells 1;
MDR-TB: Multidrug-resistant tuberculosis;
The World Health Organization (WHO) estimated approximately one- third of the world’s population is infected with Mycobacterium tuberculosis (MTB) and active disease with human immunodeficiency virus type 1 (HIV-1) infection, mainly in Africa. HIV co-infection is known risk factor for progression of M. tuberculosis infection to active disease and increasing the risk of latent TB reactivation. HIV and tuberculosis (TB) co-infections have an immense health problem in diagnostic and therapeutic challenges [1-4]. In M. tuberculosis and HIV co infection, both potentiate and accelerating one another in deterioration of immunological functions resulting in premature death of infected host, ifuntreated.
HIV infection is the depletion of CD4+ T cells. The immunopathogenic features together systemic and chronic state of immune activation accelerated T cell contribute to the progression of HIV disease and the loss of immune balance between Th17 and regulatory T cells (Treg) during HIV disease. Cell-mediated immunity during M. tuberculosis infection is essential for control of activation of both CD4+ and CD8+ T cells [5-7]. T cells recruited to the infected lung are thought to control infection by producing IFN-γ in response to mycobacterial antigens presented by macrophages. It has been reported that DC-SIGN, a dendritic cell-specific HIV-1-binding protein that enhances trans- infection of T cells [8]. An immune reconstitution inflammatory syndrome (IRIS) develops in M. tuberculosis and HIV co- infected patients undergo anti-TB treatment and antiretroviral therapy (ART) [9, 10]. TB patients present with an exacerbation of symptoms and radiological manifestations recognize predictors of IRIS in low CD4+ T lymphocyte counts and high plasma viral load prior to initiation of ART. CD4+ counts increase after highly active antiretroviral therapy (HAART) onset.
Though combination antiretroviral therapy (ART) has significantly improved the clinical outcome, they develop hyper inflammatory reactions. Antiretroviral treatment (ART) reduces the risk of developing active tuberculosis (TB) in HIV-1 co-infected patients. RNAseq analysis of whole blood-derived RNA from individuals with latent TB infection co-infected with HIV-1, a significant fall in RNA sequence abundance of the Hallmark IFN-α, IFN-γ, IL-6/JAK/STAT3 signaling to indicate reduced immune activation and inflammation. ART-induced decrease in immune activation combined with the improved antigen responsiveness, contributes to reduced susceptibility to tuberculosis in HIV-1/Mtb co- infected persons.
Based on different roles of cytokines in HIV-1, tuberculosis (TB) and co- infection during the disease and the therapy is described in the present review.
Cytokine roles in HIV, Tuberculosis and HIV-1 Tuberculosis co-infection
Interleukin-2 (IL-2) role. IL-2 cytokine is a glycoprotein that stimulates the growth of T cell lymphocytes. The major sources of IL-2 are activated CD4+ and CD8+ T cells. HIV-1 interactions implicate the gradual loss of IL-2 secretionand proliferation. It is an early sign of T cell exhaustion in HIV-1 infection. T-helper type 1 (Th1) cytokines such as IL-2 and the antiviral IFN-γ decrease duringthe course of HIV-1 infection [11]. IL-2 can simultaneously activate T effectorcells and Foxp3(+) Treg populations. It confers resistance to severe TB without enhancing M. tuberculosis infection. IL-2-producing Mtb-specific CD4 T cells Th1 cytokines IFN-γ and/or TNF-α are associated with individuals with latent tuberculosis. The Mtb containment high proportion of Mtb-specific CD4 T cells producing Th1 cytokines in the absence of IL-2 are associated with patients suffering from active TB disease [12]. HIV/TB co-infected patients of TB latency targeted by HIV-1 infection, resulting in early peripheral depletion of MTB-specific CD4+ T cells after HIV infection. Anti-tubercular treatment (ATT) associated with changes in the phenotype of Mtb-specific CD4 T cells with decreased expression of HLA-DR and increased CD27 and CD153 expression [13]. Polyfunctional T cell responses of IFN-γ (+) IL-2 (+) TNF-α (+) to TB antigens has been observed in HIV-1-infected patients dependent on their TB status, CD4 counts, and anti-retroviral exposure [14].
Interleukin-4 (IL-4) role. IL-4 is a cytokine that stimulates the proliferation of activated B-cells. It inducesdifferentiation of naivehelper T cells (Th0 cells) to Th-2 cells.IL-4 stimulates the expression of all HIV-
1 isolates via a transcriptional activation mechanism. HIV infection functionally impairs Mycobacterium tuberculosis-specific CD4 and CD8 T-cell responses. HIV infection significantly reduced the Th2 (interleukin 4 [IL-4]/IL-5/IL-13) producingM. tuberculosis-specific CD4 T cells [15]. Blocking IL-4 cause significantly neutralized Mycobacterium containment and CD4+ IFNγ+ levels Treg expression. IL-4 can subvert mycobacterial containment in human macrophages, probably via perturbations in Treg and Th1-linked pathways[16].
Interleukin-6 (IL-6) role. IL-6 interleukin acts as both a pro- inflammatory cytokine and an anti-inflammatory myokine. IL-6 is secreted by macrophages in response to specific microbial molecules, referred to as pathogen-associated molecular patterns (PAMPs). In HIV- 1 antibody positive patients, no correlation between IL-6 concentrations and CD4 positive cell numbers but a correlation with IgG. HIV-induced IL-6/IL-10 dysregulation of CD4 cells is associated with defective B cell help and autoantibody formation against CD4 cells [17]. In anti-TB treatment, a reduction in the percentage of CD4+ T cells showed a significant restoration similar to that of controls.Moreover, after intensive anti-TB treatment, serum levels of IL-1β, soluble interleukin-2 receptor, IL-6, and tumour necrosisfactor-α were significantly decreased compared with before treatment [18]. The HIV envelope glycoprotein gp160 support B cell differentiation. T cell dependence for gp160-induced B cell differentiation responses requires contact-dependent interaction of several cell surface molecules and IL-6 secretion [19].
Interleukin-10 (IL-10) role. IL-10 is an anti-inflammatory cytokine, which is primarily produced by monocytes, and lesser extent by type-II T helper cells (TH2) lymphocytes, mast cells, CD4+CD25+Foxp3+ regulatory T cells and certain subset of activated T cells and B cells. The inhibitory effectsof IL-10 on HIV-1 replication become more pronounced in late stages of disease when CD4+ lymphocytes are depleted and replication in macrophages and monocytes. Interleukin-10 induced by human immunodeficiency virus type 1 and its gp120 protein in human monocytes/macrophages. Interleukin-10 influenced promoter polymorphisms on HIV-1 susceptibility pathogenesis and play a role by transcriptional regulation [20-22].
HIV induces the immunosuppressive IL-10 production in monocytes that interferes with HIV entry through CD4 molecules. IL-10 is a more potent inhibitor than TGF-β for both T-cell subsets CD4 (+) and CD8 (+) T-cell responses to M. tuberculosis infection control [23].
IL 10 production by macrophages and T-cells during the course of Mtb is observed to increaseCD4 T cell counts and suppression of HIV viral load for all patients under HAART and TB treatment. Descendent trajectories were observed for the activated CD8 (+)/CD38 (+) and CD3 (+)/HLA- DR (+) T cell subsets, and for plasma concentration of gamma- interferon (IFN-γ) in tuberculosis and HIV-positive individuals during antituberculous treatment [24].
Interleukin-12(IL-12) role. IL-12 is a naturally produced by dendritic cells, macrophages, neutrophils, and human B-lymphoblastoid. IL-12 family is unique heterodimeric cytokines, which includes IL-12, IL-23, IL-27 and IL-35. HIV-1 infection dysregulate regulatory pathways are characterized by decreased production of IL-12 and IFN-γ pro- inflammatory cytokines. The inhibition of IL-12 production by accessory cells after HIV-1 infection has been identified as a potential factor responsible for impairedinnate and Th1 cell-mediated responses in AIDS patients. There was found a decreased CD40 ligand in CD4 T cells dependent IL-12 production in HIV-1 infection [25]. Human IL-12 and IL-23 are both required for optimal IFN-γ-dependent immunity to mycobacteria [26]. Systemic immune activation is critical to the pathogenesis of HIV-1 disease, and is accentuated in HIV/TB co-infected patients. The contribution of immune activation at sites of HIV/TB co- infection to viral activity, CD4 T cell count, and productive HIV-1 infection were measured markers of immune activation both in pleural fluid and plasma in HIV/TB co-infected subjects.
Interleukin-15 (IL-15) role. IL-15 is a cytokine similar to IL-2. IL-15 binds to signals through IL-2/IL-15 receptor beta chain (CD122) and the common gamma chain (gamma-C, CD132). IL-15 is secreted by mononuclear phagocytes. IL-15 regulates susceptibility of CD4 + T cells to HIV infection. IL-15 level was significantly elevated viral loads in HIV-1 infected patients compared to uninfected controls, suggesting a significant direct correlation between IL-15 and HIV-1 viraemia and an inverse correlation between IL-15 levels and CD4+ T cell counts [27]. NK cells produce not only IFN-γ but also IL-22 induced by IL-15 and DAP-10. Many invariant natural killer T (iNKT) cells are CD4+ and few iNKT cells are CD8+. Other iNKT cells are negative for both CD4 and CD8. Gamma Delta (γδ) T cells represents an early innate defense anti- mycobacterial immunity [28]. As NK cells are a significant source of the bactericidal effector molecule granulysin, infection of PBMC (peripheral blood mononuclear cell) with HIV-1 suppresses NK cell induction of granulysin by IL-15, but does not impair activation by BCG. This study suggests that HIV impair the anti-bacterial function of NK cells and have implications for clinical use of IL-15 to augment innate cell mediated immunity in HIV positive patients [29].
Interleukin-17 (IL-17) role. IL-17 is a pro-inflammatory cytokine. IL- 17 is a unique CD4+ T (Th17)cell subset play a role in host defense. Th17 cells are lost duringHIV infection, althoughthere is also a beneficial role of HIV-specific CD4 cells. Patients with lower immune activation exhibited higher frequency of bulk CD4 T-cells producing IFN-γ or IL-
17 which change higher effector-to-regulatory cell ratios [30, 31]. Although initial studies suggested that γδ T cells are a primary source of IL-17 in response to M. tuberculosis infection [32]. Th17 cells are the major IL-17–producing cells and participate in the protective immunity against M. tuberculosis. The high proportion of CD4 (+) IFN-γ (+) IL- 17(+) cells were detected in low responder TB patients with severe pulmonary lesions [33]. The cytokine frequency and polyfunctionality profile of Mycobacterium tuberculosis (MTB)-specific CD4+ T cells in HIV-infected persons with latent TB infection (LTBI) or Pulmonary TB (PTB) is comparable. This similarity suggests that LTBI represent a smoldering state of persistent MTB replication rather than dormant infection [34].
Interleukin-18 (IL-18) role. IL-18 is a pro-inflammatory cytokine. It is also known as IFN-γ inducing factor. Both hematopoietic cells and non- hematopoietic cells have the potential to produce IL-18. IL-18 brings an alteration in the immune response to tuberculosis (TB). Mycobacterial antigen-induced production plasma levels of inflammatory cytokine IFN- γand its regulatory cytokines IL-18, and IL-12, IL-10 in HIV co-infected with TB patients. Patients with multidrug-resistant TB (MDRTB) have dysregulated IL-12, IL-18 and IL-10 production during Mycobacterium tuberculosis.
Interleukin-22 (IL-22) role. HIV infection indicates a gradual loss of CD4+ T-cellswith progressive impairment of immunity lead ultimately to death. Study of IL-22+ cells of HIV-1 co-infected with Mycobacterium tuberculosis patients detect the levels of peripheral blood membrane- bound IL-22+ T cell subsets. Antigen-specific membrane-bound IL-22+ T cells are highly expressed in MTB co-infection of HIV-1 infected individuals, and play an important role in anti-TB immune response during co-infection with HIV-1 [35]. In multidrug-resistant TB (MDR- TB), low systemic and Mtb-induced Th22 responses associated with a high sputum bacillary load and bilateralism of lung lesions, suggesting that Th22 response could be influencing the ability of MDR-TB patients to control bacillary growth and tissue damage. The level of IL-22 and IFN-γ were significantly lower in the pleural fluid of HIV-1 co-infected TB than the TB patients. Antigen-specific membrane-bound IL-22+ T cells are highly expressed in MTB co-infection of HIV-1 and play anti- TB immune response. Proteomics analyses revealed the enrichment of HIF-1α, galectins and Hsp90 host factors, which promoted HIV-1 reactivation M. tuberculosis-specific exosomes [36]. Tuberculosis (TB) and AIDS are the leading causes of death, but in some TB-HIV co- infected individuals treated for both diseases simultaneously, an inflammatory reaction termed immune reconstitution inflammatory syndrome (IRIS) occur.
Interleukin-27 (IL-27) role. IL-27 is a heterodimeric cytokine and a member of the IL-12 family. IL-27 has been shown to be a potent inhibitor of HIV-1 infection in CD4+ T cells and macrophages. IL-27 treated dendritic cells (DCs) have shown highly potent inhibitors of HIV- 1, whereas IL-12, IL-23 and IL-35 have no effect on HIV-1 replication. IL-27-producing CD4 (+) T cells represent a distinct T cell subset in tuberculosis pleural effusion (TPE). Both the numbers of IL-27- producing CD4 (+) T cells and concentration of soluble IL-27 have been found to be increased in tuberculous pleural effusion (TPE). In HIV- infected, the plasma IL-27 level correlates positively with CD4+ T-cell count and negatively with HIV- viral load. IL-27 in HIV- M. tuberculosis co-infection acts on MDSC both in autocrine and paracrine manner. HIV-infected individuals with virologic suppression have increased levels of circulating IL-27 and myeloid-derived suppressor cells (MDSC). IL-27/IL-27R and MDSC provide attractive biomarkers to assess tuberculosis prognosis during HIV-infection[37].
Interleukin-32 (IL-32) role. IL-32 is inflammatory and clinical markers, expressed during HIV-1 infection in CD4+ T cells, B cells, macrophages, and dendritic cells. Increased expression of IL-32 seen with IFN-γ, Th1 and Tc1 in virologically suppressed HIV-1-infected patients. IL-32 is highly expressed in the mucosal epithelium of HIV-1- infected gut. IL-32's action on IFN-γ and IFN-γ secreting T cell subsets help sustain the immune activation and dysregulation found in patients with HIV-1 achieving viral suppression. Both IL-32 and IFN-γ genes were also more strongly expressed in CD4+ T cells than in CD14+ monocytes. IL-32 levels remain elevated in treating HIV-1-infected patients [38].
Interleukin-35 (IL-35) role. IL-35 is anti-inflammatory cytokine from the IL-12 family. IL-35 is produced by a wide range of regulatory lymphocytes and plays a role in immunesuppression. IL-35 can block the development of Th1 and Th17 cells by limiting early T cell proliferation. Little is known for IL-35 response in patients with active tuberculosis (ATB). Active tuberculosis patients exhibited increases in serum IL-35 and in mRNA expression of both subunits of IL-35 (p35 and EBI3) in white blood cells and peripheral blood mononuclear cells. TB infection was associated with expression of p35 or EBI3 proteinin CD4 (+) but not CD8 (+) T cells. Most p35 (+) CD4 (+) T cells and EBI3 (+) CD4 (+) T cells expressed Treg-associated marker CD25. IL-35 in the blood serves as a biomarker for immune status and prognosis in TB [39].
Immune mechanism in HIV co-infection Tuberculosis therapy
Tuberculosis is a serious health threat, especially for people living with HIV. HIV virus increases the potency of the tuberculosis bacterium (Mtb) by affecting a central function of the immune system. In HIV infected individuals, CD38 and HLA-DR on CD4 and CD8 T lymphocytes are elevated immune reconstitution inflammatory syndrome (IRIS). In response to antiretroviral therapy-mediated recovery of the immune system in HIV-infected patients, it was seen effects of initiating efavirenz (EFV) or raltegravir (RAL)-based antiretroviral therapy (ART) regimens HIV-1 deoxyribonucleic acid (DNA) levels and inflammation biomarkers in the highly inflammatory setting of advanced HIV-1 disease with tuberculosis (TB) co-infection [40].
TB treatment in HIV-TB co-infected persons have a prolonged duration due to the immune system fails to provide an adequate support for the therapy. 7-oxo-DHEA modifies the cytokine balance and the phenotype of CD4 + T cells more favorable to mycobacteria control where novel treatment approaches as co-adjuvant for the treatment of TB [41]. Thalidomide, which inhibits monocyte TNF-α production and co- stimulates T cells, was tested for immune modulation in patients with human immunodeficiency virus HIV infection and TB. Thalidomide therapy resulted in increased levelsof plasma IL-2 receptor, solubleCD8, IFN-γ, and IL-12. Thalidomide treatment increased CD4+ and CD8+ T cell counts and increased viral replication [42].
Combination antiretroviral therapy in tuberculosis (TB) and HIV-1 infection is associated with an immune reconstitution inflammatory syndrome (TB-IRIS). In serum, higher concentrations of TNF, IL-6, and IFN-γ were observed with TB-IRIS patients. Serum IL-6 and TNF-α decreased during prednisone therapy in TB-IRIS patients. It also showed increased IL-1β, IL-2, IL-6, IL-8, IL-10, IL-12p40, IFN-γ, GM-CSF and
TNF in TB-IRIS cultures in peripheral blood mononuclear cell culture in the presence of heat-killed Mycobacterium tuberculosis [43].
HIV-1 patients co-infected with some pathogens are at risk ofdeveloping the IRIS when initiating antiretroviral therapy (ART). HIV-TB co- infected patients prescribed with anti-tuberculosis treatment and ART develop TB-IRIS [44].TB-IRIS patients and controls had similar CD4 counts, levels of T-cell-associated immune activation, and frequencies of IFN-γ(+)/IL-2(+)/TNF-α(+),CD4(+) T-cells prior to ART initiation. After ART initiation, cellular immune activation and T-cell subsets also were similar in TB-IRIS patients and controls. In contrast, TB-IRIS patients had significantly greater early increases in the IFN-γ (+)/IL-2 (+)/TNF-α (+)CD4(+) T-cells in ART and increases IL-6 is associated with the development of paradoxical TB-IRIS [45].
There is a high prevalence of drug-resistant mutations in HIV and HIV- TB co-infected patients. In the HIV-TB group had mutations to nucleoside reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), and protease inhibitors (PIs), respectively.Silencing of the expression of the nuclearfactor of activated T cells 5 (NFAT5) by RNA interference (RNAi) inhibits Mycobacterium tuberculosis (MTb)-stimulated HIV-1 replication in co-infected macrophages. NFAT5 gene and protein expression are stronglyinduced by MTb, which is a Toll-like receptor (TLR) ligand RNAi key components of the TLR pathway in human monocytes, including the downstream signaling molecules MyD88, IRAK1, and TRAF6, significantly inhibits MTb-induced NFAT5 gene expression [46]. SOCS1 factor or IL-27 down-regulate the IFN-γ/IL-12 axis, thereby impairing control are mainly anti-inflammatory but indirectly inhibit efficient bacterial clearance. Increased replication of the virus was demonstrated in the lungs and within activated lymphocytes and CD14+ macrophages of the pleural space in M. tuberculosis infection. The suppressor of cytokine signaling 1 (SOCS1) is an inducible host factor during HIV-1 infection and regulates the late stages of the HIV-1 replication pathway. The function of many immune cells, including macrophages and DCs, is modulated by both HIV and M. tuberculosis. Increased replication of the virus was demonstrated locally, at sites of M tuberculosis infection in the lung, and within activated cells, including lymphocytes and CD14 + macrophages, of the pleural space of co-infected patients [47,48].
Impaired balance between pro-inflammatory and anti-inflammatory cytokines and apoptosis-induced depletion of immune effector cells accounts for the dissemination of both the pathogens and for a poor granulomatous reaction in Mtb-HIV co-infected patients [49]. Patients with HIV-associated tuberculosis (TB) initiating antiretroviral therapy (ART) develop an immune reconstitution inflammatory syndrome (TB- IRIS), the signature is characterized by over-representation of TLR signalling and TREM-1 activation of the inflammasome. Inhibition of MyD88 adaptor and group 1 caspases reduces secretion of IL-1 in TB- IRIS patients [50].
Various cytokines play different roles in HIV-1 and TB individually and in a co-infection stage of disease during infection. IL-2 play CD4+ proliferation, IL-4 activate B cells, CD4 cell IL-6/IL-10 dysregulate in HIV-1, CD4+ T (Th17) cell subset lost during HIV-1, IL-22 and IL-27- producing CD4(+) T cells represent a distinct T cell subset in tuberculous pleural effusion (TPE). It was seeing the effects of initiating efavirenz (EFV) or raltegravir (RAL)-based antiretroviral therapy (ART) regimens on human immunodeficiency virus (HIV)-1 deoxyribonucleic acid (DNA) levels and inflammation biomarkers in the highly inflammatory setting of advanced HIV-1 disease with tuberculosis (TB) co-infection.
HIV co infected TB patients have prolonged treatmentduration due to the immune system failing to provide support for the therapy. HIV co- infected TB patients have mutations to nucleoside reverse transcriptase, inhibits MTb-induced NFAT5 gene expression. It was noted that bacteria are not completely eradicated despite of a seemingly robust Th1 immune response in the latent phase of tuberculosis. A failure of the protective adaptive immune responses leads to reactivation of infection.
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I am delighted to publish our manuscript entitled "A Perspective on Cocaine Induced Stroke - Its Mechanisms and Management" in the Journal of Neuroscience and Neurological Surgery. The peer review process, support from the editorial office, and quality of the journal are excellent. The manuscripts published are of high quality and of excellent scientific value. I recommend this journal very much to colleagues.
Dr.Tania Muñoz, My experience as researcher and author of a review article in The Journal Clinical Cardiology and Interventions has been very enriching and stimulating. The editorial team is excellent, performs its work with absolute responsibility and delivery. They are proactive, dynamic and receptive to all proposals. Supporting at all times the vast universe of authors who choose them as an option for publication. The team of review specialists, members of the editorial board, are brilliant professionals, with remarkable performance in medical research and scientific methodology. Together they form a frontline team that consolidates the JCCI as a magnificent option for the publication and review of high-level medical articles and broad collective interest. I am honored to be able to share my review article and open to receive all your comments.
“The peer review process of JPMHC is quick and effective. Authors are benefited by good and professional reviewers with huge experience in the field of psychology and mental health. The support from the editorial office is very professional. People to contact to are friendly and happy to help and assist any query authors might have. Quality of the Journal is scientific and publishes ground-breaking research on mental health that is useful for other professionals in the field”.
Dear editorial department: On behalf of our team, I hereby certify the reliability and superiority of the International Journal of Clinical Case Reports and Reviews in the peer review process, editorial support, and journal quality. Firstly, the peer review process of the International Journal of Clinical Case Reports and Reviews is rigorous, fair, transparent, fast, and of high quality. The editorial department invites experts from relevant fields as anonymous reviewers to review all submitted manuscripts. These experts have rich academic backgrounds and experience, and can accurately evaluate the academic quality, originality, and suitability of manuscripts. The editorial department is committed to ensuring the rigor of the peer review process, while also making every effort to ensure a fast review cycle to meet the needs of authors and the academic community. Secondly, the editorial team of the International Journal of Clinical Case Reports and Reviews is composed of a group of senior scholars and professionals with rich experience and professional knowledge in related fields. The editorial department is committed to assisting authors in improving their manuscripts, ensuring their academic accuracy, clarity, and completeness. Editors actively collaborate with authors, providing useful suggestions and feedback to promote the improvement and development of the manuscript. We believe that the support of the editorial department is one of the key factors in ensuring the quality of the journal. Finally, the International Journal of Clinical Case Reports and Reviews is renowned for its high- quality articles and strict academic standards. The editorial department is committed to publishing innovative and academically valuable research results to promote the development and progress of related fields. The International Journal of Clinical Case Reports and Reviews is reasonably priced and ensures excellent service and quality ratio, allowing authors to obtain high-level academic publishing opportunities in an affordable manner. I hereby solemnly declare that the International Journal of Clinical Case Reports and Reviews has a high level of credibility and superiority in terms of peer review process, editorial support, reasonable fees, and journal quality. Sincerely, Rui Tao.
Clinical Cardiology and Cardiovascular Interventions I testity the covering of the peer review process, support from the editorial office, and quality of the journal.
Clinical Cardiology and Cardiovascular Interventions, we deeply appreciate the interest shown in our work and its publication. It has been a true pleasure to collaborate with you. The peer review process, as well as the support provided by the editorial office, have been exceptional, and the quality of the journal is very high, which was a determining factor in our decision to publish with you.
The peer reviewers process is quick and effective, the supports from editorial office is excellent, the quality of journal is high. I would like to collabroate with Internatioanl journal of Clinical Case Reports and Reviews journal clinically in the future time.
Clinical Cardiology and Cardiovascular Interventions, I would like to express my sincerest gratitude for the trust placed in our team for the publication in your journal. It has been a true pleasure to collaborate with you on this project. I am pleased to inform you that both the peer review process and the attention from the editorial coordination have been excellent. Your team has worked with dedication and professionalism to ensure that your publication meets the highest standards of quality. We are confident that this collaboration will result in mutual success, and we are eager to see the fruits of this shared effort.
Dear Dr. Jessica Magne, Editorial Coordinator 0f Clinical Cardiology and Cardiovascular Interventions, I hope this message finds you well. I want to express my utmost gratitude for your excellent work and for the dedication and speed in the publication process of my article titled "Navigating Innovation: Qualitative Insights on Using Technology for Health Education in Acute Coronary Syndrome Patients." I am very satisfied with the peer review process, the support from the editorial office, and the quality of the journal. I hope we can maintain our scientific relationship in the long term.
Dear Monica Gissare, - Editorial Coordinator of Nutrition and Food Processing. ¨My testimony with you is truly professional, with a positive response regarding the follow-up of the article and its review, you took into account my qualities and the importance of the topic¨.
Dear Dr. Jessica Magne, Editorial Coordinator 0f Clinical Cardiology and Cardiovascular Interventions, The review process for the article “The Handling of Anti-aggregants and Anticoagulants in the Oncologic Heart Patient Submitted to Surgery” was extremely rigorous and detailed. From the initial submission to the final acceptance, the editorial team at the “Journal of Clinical Cardiology and Cardiovascular Interventions” demonstrated a high level of professionalism and dedication. The reviewers provided constructive and detailed feedback, which was essential for improving the quality of our work. Communication was always clear and efficient, ensuring that all our questions were promptly addressed. The quality of the “Journal of Clinical Cardiology and Cardiovascular Interventions” is undeniable. It is a peer-reviewed, open-access publication dedicated exclusively to disseminating high-quality research in the field of clinical cardiology and cardiovascular interventions. The journal's impact factor is currently under evaluation, and it is indexed in reputable databases, which further reinforces its credibility and relevance in the scientific field. I highly recommend this journal to researchers looking for a reputable platform to publish their studies.
Dear Editorial Coordinator of the Journal of Nutrition and Food Processing! "I would like to thank the Journal of Nutrition and Food Processing for including and publishing my article. The peer review process was very quick, movement and precise. The Editorial Board has done an extremely conscientious job with much help, valuable comments and advices. I find the journal very valuable from a professional point of view, thank you very much for allowing me to be part of it and I would like to participate in the future!”
Dealing with The Journal of Neurology and Neurological Surgery was very smooth and comprehensive. The office staff took time to address my needs and the response from editors and the office was prompt and fair. I certainly hope to publish with this journal again.Their professionalism is apparent and more than satisfactory. Susan Weiner
My Testimonial Covering as fellowing: Lin-Show Chin. The peer reviewers process is quick and effective, the supports from editorial office is excellent, the quality of journal is high. I would like to collabroate with Internatioanl journal of Clinical Case Reports and Reviews.
My experience publishing in Psychology and Mental Health Care was exceptional. The peer review process was rigorous and constructive, with reviewers providing valuable insights that helped enhance the quality of our work. The editorial team was highly supportive and responsive, making the submission process smooth and efficient. The journal's commitment to high standards and academic rigor makes it a respected platform for quality research. I am grateful for the opportunity to publish in such a reputable journal.
My experience publishing in International Journal of Clinical Case Reports and Reviews was exceptional. I Come forth to Provide a Testimonial Covering the Peer Review Process and the editorial office for the Professional and Impartial Evaluation of the Manuscript.
I would like to offer my testimony in the support. I have received through the peer review process and support the editorial office where they are to support young authors like me, encourage them to publish their work in your esteemed journals, and globalize and share knowledge globally. I really appreciate your journal, peer review, and editorial office.
Dear Agrippa Hilda- Editorial Coordinator of Journal of Neuroscience and Neurological Surgery, "The peer review process was very quick and of high quality, which can also be seen in the articles in the journal. The collaboration with the editorial office was very good."
I would like to express my sincere gratitude for the support and efficiency provided by the editorial office throughout the publication process of my article, “Delayed Vulvar Metastases from Rectal Carcinoma: A Case Report.” I greatly appreciate the assistance and guidance I received from your team, which made the entire process smooth and efficient. The peer review process was thorough and constructive, contributing to the overall quality of the final article. I am very grateful for the high level of professionalism and commitment shown by the editorial staff, and I look forward to maintaining a long-term collaboration with the International Journal of Clinical Case Reports and Reviews.
To Dear Erin Aust, I would like to express my heartfelt appreciation for the opportunity to have my work published in this esteemed journal. The entire publication process was smooth and well-organized, and I am extremely satisfied with the final result. The Editorial Team demonstrated the utmost professionalism, providing prompt and insightful feedback throughout the review process. Their clear communication and constructive suggestions were invaluable in enhancing my manuscript, and their meticulous attention to detail and dedication to quality are truly commendable. Additionally, the support from the Editorial Office was exceptional. From the initial submission to the final publication, I was guided through every step of the process with great care and professionalism. The team's responsiveness and assistance made the entire experience both easy and stress-free. I am also deeply impressed by the quality and reputation of the journal. It is an honor to have my research featured in such a respected publication, and I am confident that it will make a meaningful contribution to the field.
"I am grateful for the opportunity of contributing to [International Journal of Clinical Case Reports and Reviews] and for the rigorous review process that enhances the quality of research published in your esteemed journal. I sincerely appreciate the time and effort of your team who have dedicatedly helped me in improvising changes and modifying my manuscript. The insightful comments and constructive feedback provided have been invaluable in refining and strengthening my work".
I thank the ‘Journal of Clinical Research and Reports’ for accepting this article for publication. This is a rigorously peer reviewed journal which is on all major global scientific data bases. I note the review process was prompt, thorough and professionally critical. It gave us an insight into a number of important scientific/statistical issues. The review prompted us to review the relevant literature again and look at the limitations of the study. The peer reviewers were open, clear in the instructions and the editorial team was very prompt in their communication. This journal certainly publishes quality research articles. I would recommend the journal for any future publications.
Dear Jessica Magne, with gratitude for the joint work. Fast process of receiving and processing the submitted scientific materials in “Clinical Cardiology and Cardiovascular Interventions”. High level of competence of the editors with clear and correct recommendations and ideas for enriching the article.
We found the peer review process quick and positive in its input. The support from the editorial officer has been very agile, always with the intention of improving the article and taking into account our subsequent corrections.
My article, titled 'No Way Out of the Smartphone Epidemic Without Considering the Insights of Brain Research,' has been republished in the International Journal of Clinical Case Reports and Reviews. The review process was seamless and professional, with the editors being both friendly and supportive. I am deeply grateful for their efforts.
To Dear Erin Aust – Editorial Coordinator of Journal of General Medicine and Clinical Practice! I declare that I am absolutely satisfied with your work carried out with great competence in following the manuscript during the various stages from its receipt, during the revision process to the final acceptance for publication. Thank Prof. Elvira Farina
Dear Jessica, and the super professional team of the ‘Clinical Cardiology and Cardiovascular Interventions’ I am sincerely grateful to the coordinated work of the journal team for the no problem with the submission of my manuscript: “Cardiometabolic Disorders in A Pregnant Woman with Severe Preeclampsia on the Background of Morbid Obesity (Case Report).” The review process by 5 experts was fast, and the comments were professional, which made it more specific and academic, and the process of publication and presentation of the article was excellent. I recommend that my colleagues publish articles in this journal, and I am interested in further scientific cooperation. Sincerely and best wishes, Dr. Oleg Golyanovskiy.
Dear Ashley Rosa, Editorial Coordinator of the journal - Psychology and Mental Health Care. " The process of obtaining publication of my article in the Psychology and Mental Health Journal was positive in all areas. The peer review process resulted in a number of valuable comments, the editorial process was collaborative and timely, and the quality of this journal has been quickly noticed, resulting in alternative journals contacting me to publish with them." Warm regards, Susan Anne Smith, PhD. Australian Breastfeeding Association.
Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. I appreciate the journal (JCCI) editorial office support, the entire team leads were always ready to help, not only on technical front but also on thorough process. Also, I should thank dear reviewers’ attention to detail and creative approach to teach me and bring new insights by their comments. Surely, more discussions and introduction of other hemodynamic devices would provide better prevention and management of shock states. Your efforts and dedication in presenting educational materials in this journal are commendable. Best wishes from, Farahnaz Fallahian.
Dear Maria Emerson, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. I am delighted to have published our manuscript, "Acute Colonic Pseudo-Obstruction (ACPO): A rare but serious complication following caesarean section." I want to thank the editorial team, especially Maria Emerson, for their prompt review of the manuscript, quick responses to queries, and overall support. Yours sincerely Dr. Victor Olagundoye.
Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews. Many thanks for publishing this manuscript after I lost confidence the editors were most helpful, more than other journals Best wishes from, Susan Anne Smith, PhD. Australian Breastfeeding Association.
Dear Agrippa Hilda, Editorial Coordinator, Journal of Neuroscience and Neurological Surgery. The entire process including article submission, review, revision, and publication was extremely easy. The journal editor was prompt and helpful, and the reviewers contributed to the quality of the paper. Thank you so much! Eric Nussbaum, MD
Dr Hala Al Shaikh This is to acknowledge that the peer review process for the article ’ A Novel Gnrh1 Gene Mutation in Four Omani Male Siblings, Presentation and Management ’ sent to the International Journal of Clinical Case Reports and Reviews was quick and smooth. The editorial office was prompt with easy communication.
Dear Erin Aust, Editorial Coordinator, Journal of General Medicine and Clinical Practice. We are pleased to share our experience with the “Journal of General Medicine and Clinical Practice”, following the successful publication of our article. The peer review process was thorough and constructive, helping to improve the clarity and quality of the manuscript. We are especially thankful to Ms. Erin Aust, the Editorial Coordinator, for her prompt communication and continuous support throughout the process. Her professionalism ensured a smooth and efficient publication experience. The journal upholds high editorial standards, and we highly recommend it to fellow researchers seeking a credible platform for their work. Best wishes By, Dr. Rakhi Mishra.
Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. The peer review process of the journal of Clinical Cardiology and Cardiovascular Interventions was excellent and fast, as was the support of the editorial office and the quality of the journal. Kind regards Walter F. Riesen Prof. Dr. Dr. h.c. Walter F. Riesen.
Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. Thank you for publishing our article, Exploring Clozapine's Efficacy in Managing Aggression: A Multiple Single-Case Study in Forensic Psychiatry in the international journal of clinical case reports and reviews. We found the peer review process very professional and efficient. The comments were constructive, and the whole process was efficient. On behalf of the co-authors, I would like to thank you for publishing this article. With regards, Dr. Jelle R. Lettinga.
Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, I would like to express my deep admiration for the exceptional professionalism demonstrated by your journal. I am thoroughly impressed by the speed of the editorial process, the substantive and insightful reviews, and the meticulous preparation of the manuscript for publication. Additionally, I greatly appreciate the courteous and immediate responses from your editorial office to all my inquiries. Best Regards, Dariusz Ziora
Dear Chrystine Mejia, Editorial Coordinator, Journal of Neurodegeneration and Neurorehabilitation, Auctores Publishing LLC, We would like to thank the editorial team for the smooth and high-quality communication leading up to the publication of our article in the Journal of Neurodegeneration and Neurorehabilitation. The reviewers have extensive knowledge in the field, and their relevant questions helped to add value to our publication. Kind regards, Dr. Ravi Shrivastava.
Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, Auctores Publishing LLC, USA Office: +1-(302)-520-2644. I would like to express my sincere appreciation for the efficient and professional handling of my case report by the ‘Journal of Clinical Case Reports and Studies’. The peer review process was not only fast but also highly constructive—the reviewers’ comments were clear, relevant, and greatly helped me improve the quality and clarity of my manuscript. I also received excellent support from the editorial office throughout the process. Communication was smooth and timely, and I felt well guided at every stage, from submission to publication. The overall quality and rigor of the journal are truly commendable. I am pleased to have published my work with Journal of Clinical Case Reports and Studies, and I look forward to future opportunities for collaboration. Sincerely, Aline Tollet, UCLouvain.
Dear Ms. Mayra Duenas, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews. “The International Journal of Clinical Case Reports and Reviews represented the “ideal house” to share with the research community a first experience with the use of the Simeox device for speech rehabilitation. High scientific reputation and attractive website communication were first determinants for the selection of this Journal, and the following submission process exceeded expectations: fast but highly professional peer review, great support by the editorial office, elegant graphic layout. Exactly what a dynamic research team - also composed by allied professionals - needs!" From, Chiara Beccaluva, PT - Italy.
Dear Maria Emerson, Editorial Coordinator, we have deeply appreciated the professionalism demonstrated by the International Journal of Clinical Case Reports and Reviews. The reviewers have extensive knowledge of our field and have been very efficient and fast in supporting the process. I am really looking forward to further collaboration. Thanks. Best regards, Dr. Claudio Ligresti
