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The expression of programmed cell death protein-1 (PD-1) and its ligands- PD-L1 and PD-L2- on T cells and macrophages', respectively, increases in Leishmania infection. The PD-1/PD-L1 interaction induces T cell anergy, T cell apoptosis and exhaustion, diversion of T cells toward T

Infection with the same species of Leishmania (L)donovani causes different manifestations including visceral leishmaniasis (VL) and post kala-azar dermal leishmaniasis (PKDL), indicating that the host-related immunological parameters perform a decisive role in the pathogenesis of diseases. As PKDL is a reservoir of the parasite, a better understanding of the host immune responses is necessary to restrict the L. donovani transmission. The proper local production of Th1 cell-related cytokines (including IFN-γ, TNF-α and IL-12), Th17 cell-derived cytokines (such as IL-17A, IL-17F and IL-22), and CD8+ cytotoxic T lymphocyte (CTL)-derived IFN-γ are protective against PKDL. However, dominant production of regulatory CD4+ T cell-derived cytokines (such as IL-10 and TGF-β), Th2 cell-derived cytokines (such as IL-4/IL-13), M2 macrophage-derived cytokines (such as IL-4 and IL-10), keratinocyte-derived IL-10, regulatory CD8+ T cell-derived IL-10, and dendritic cell-derived IL-10, IL-27 and IL-21 can contribute to the parasite persistence and PKDL development. Understanding of the T cell-related cytokine network within PKDL lesions gives rise to novel insights concerning the role of each cytokine in the protection or susceptibility to disease. Manipulation of the cytokine network can be considered as an interesting immunotherapeutic strategy for the treatment of L. donovani-mediated PKDL.

The immunopathologic responses play a major role in the development of H. pylori (HP)-related gastrointestinal diseases. IL-37 is an anti-inflammatory cytokine with potent suppressive effects on innate and adaptive immune responses. Here, we investigated the IL-37 levels and two single nucleotide polymorphisms (SNPs) including rs3811047 and rs2723176 in IL-37 gene in HP-infected peptic ulcer (PU) patients to identify any relationship. Three groups, including 100 HP-infected PU patients, 100 HP-infected asymptomatic (AS) subjects and 100 non-infected healthy control (NHC) subjects were enrolled to study. Serum IL-37 levels and the genotyping at rs3811047 and rs2723176 were determined using ELISA and SSP-PCR methods, respectively. Significantly higher IL-37 levels were observed in PU patients compared with AS and NHC groups (P 0.0001). In both PU and AS groups, the CagA

IL-35 is an immunosuppressive cytokine that is largely synthesized by regulatory T (Treg) cells and may inhibit antitumor immune responses. This investigation aimed to determine the serum IL-35 concentrations and a single nucleotide polymorphism (SNP) in position of rs3761548, within the promoter region of FOXP3 gene, in patients with prostate cancer (PC). The blood specimens were obtained from 150 PC patients prior to using radiation therapy, chemo- or immunotherapy and 150 age-matched healthy men as a control group. The serum IL-35 concentrations and the pattern of genetic variation at position of rs3761548 were assessed using ELISA and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), respectively. The mean serum IL-35 concentrations were significantly higher in PC patients when compared with healthy control group (20.01 ± 7.03 Pg/mL vs. 11.60 ± 2.49 Pg/mL, P 0.001). The serum IL-35 concentrations raised with progression of PC stages so that there was a significant difference between PC stages concerning the IL-35 concentrations (P 0.001). The mean serum IL-35 concentrations in patients with Gleason scores of 1-6 and Gleason scores 7-10 were significantly higher as compared with healthy controls (P 0.001). Moreover, the serum IL-35 concentrations in patients with having Gleason scores of 7-10 were significantly higher as compared with patients with Gleason scores of 1-6 (P 0.001). Evaluation of the genetic variations in position SNP rs3761548 revealed that the AA genotype and A allele were more prevalent whereas CC genotype and C allele were less prevalent in PC patients when compared with healthy men (P 0.01, P 0.001, P 0.002 and P 0.001, respectively). The AA genotype and A allele were associated with higher risk of PC incidence [OR: 2.42 (95% CI: 1.179-4.99); P 0.001 and OR: 1.732 (95% CI: 1.244 - 2.413); P 0.001, respectively]. The mean serum IL-35 concentrations were significantly higher in total subjects (PC patients + healthy individuals) with AA genotype and A allele than individuals with CC genotype and C allele at SNP rs3761548 (P 0.05 and P 0.01, respectively). Higher serum IL-35 concentrations observed in patients with PC that were increased with progressive tumor stages. These findings indicate that the IL-35 is possibly involve in tumor progression. Moreover, SNP rs3761548 may affect the susceptibility to PC and the serum IL-35 concentrations.

Recruitment of leukocytes is one of the earliest events in the pathogenesis of ischemic heart disease (IHD) and chemokines play an important role in the migration of these cells into the inflammation sites. The aim of this study was to evaluate the CXCL10, CCL20 and CCL22 levels and the single nucleotide polymorphisms (SNPs) rs4508917, rs6749704 and rs4359426 in chemokine genes in patients with IHD to clarify any association. A total of 300 patients with IHD as having acute myocardial infarction (AMI; n=100), stable angina (SA; n=100) or unstable angina (UA; n=100) and 100 healthy subjects as a control group were enrolled to study. Serum samples from all participants were tested for the CXCL10, CCL20 and CCL22 levels by using ELISA. The SNPs were determined by polymerase chain reaction-restriction length polymorphism (PCR-RFLP) method. The mean serum concentrations of CXCL10, CCL20 and CCL22 in AMI patients (395.97±21.20Pg/mL, 108.38±10.31Pg/mL and 1852.58±205.77Pg/mL), SA patients (405.48±27.36Pg/mL, 90.20±7.69Pg/mL and 2322.04±231.23Pg/mL) and UA patients (396.69±22.79Pg/mL, 141.87±18.10Pg/mL and 2754.89±211.70Pg/mL) were significantly higher than in the healthy group (179.38±8.85Pg/mL, 51.92±4.62Pg/mL and 451.82±23.76Pg/mL, respectively; P

Cytokines, the key mediators of immune responses, play an important role in the pathogenesis of cardiovascular diseases. The aim of this study was to evaluate the serum levels of IL-27 in patients with ischemic heart disease (IHD) and also to clarify its association with traditional risk factors of the disease.A total of 120 patients with IHD as having acute myocardial infarction (AMI; n=60) or unstable angina (UA; n=60) and 60 sex- and age-matched healthy subjects as a control group were enrolled in this cross-sectional, case-controlled study. Serum samples were collected from all participants (for AMI patients at 3-5 days after events and for UA at admission time) and tested for the levels of IL-27 by use of ELISA method.The mean serum levels of IL-27 in AMI group (38.00±14.38 Pg/ml) and UA group (35.77±18.93 Pg/ml) were significantly higher than those observed in the control group (24.91±14.96 Pg/ml; P0.0001 and 0.001, respectively). The mean serum levels of IL-27 in IHD patients with or without a certain traditional risk factor including hypertension, dyslipidemia, diabetes smoking were significantly higher as compared to those in the control group.These results showed that the higher serum levels of IL-27 were associated with IHD. The presence or absence of certain traditional risk factors of IHD did not influence the serum levels of cytokine.