Dysfunction of regulatory T cells (Tregs) may contribute to certain immune‐related pregnancy complications. Forkhead box protein 3 (FOXP3) is the key transcription factor of Treg. We performed a systematic review and meta‐analysis to evaluate the possible association between FOXP3 polymorphisms −924A/G (rs2232365) and −3279C/A (rs3761548) and immune‐related pregnancy complications. After reviewing 78 fully published studies, 10 studies fulfilled previously defined eligibility criteria and were used for meta‐analysis. Two single nucleotide polymorphisms showed a significant correlation with increased or reduced risk for immune‐related pregnancy complications. For rs3761548, women with allele A were significantly at a higher risk than women carrying allele C (odds ratio = 1.29, 95% confidence interval: 1.20–1.38; p = 0.001). For rs2232365, women with GG or AG genotype were at a higher risk than women with genotype AA, thereby, allele G was significantly associated with a higher risk than allele A. Our meta‐analysis supports the notion that immune‐related pregnancy complications might be linked to genetic variations in the FOXP3 gene.

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Background: Helicobacter pylori is accounted as the most etiologic agent for digestive disorders, in particular, the most important of them i.e. peptic ulcer and gastric cancer. In the recent years, association of vacA genotypes and gastrointestinal disorders has attracted a lot of attention. In present study, we assessed the correlation between vacA genotypes (s1, s2, m1, m2, s1m1, s1m2, s2m1 and s2m2) and development to peptic ulcer in Iranian population. Methods: In our study, first, 24 original articles containing of information of 3328 patients were evaluated. Statistical analysis was done by Comprehensive Meta-Analysis version 2.0 software (Biostat, Englewood, NJ, USA). In this regards, we used from fixed-effects model for analysis of data with low heterogeneity, while for analysis of data with high heterogeneity (I 2 statistic index > 25%, Cochrane Q statistic p value < 0.05), random-effects model was used.

Nowadays, exposure to infectious diseases caused by pathogenic viruses has become one of the major human concerns in health fields. In the meantime, hepatitis viruses are associated with health problems, especially in liver tissue. So far, several types of these viruses have been known including: HAV, HBV, HCV, HDV, HEV, and HGV. Nevertheless, it seems that hepatitis C is the major viral infection among all of the hepatitis infections. The cirrhosis and hepatocellular carcinoma are known as the most important pathological complications of this virus, from which seven genotypes have been identified. However, among these genotypes, the incidence rate of genotypes 1 and 3 is more than others. In this review, we have investigated the relationship between all HCV genotypes and therapeutic responses against them. Regarding heterogeneity between hepatitis C genotypes, it is not possible to access an effective vaccine against this virus, and treatment is the only applicable strategy. Response to treatment is different among genotypes, and it has resulted that each genotype has a specific therapeutic regimen of itself. Therefore, it seems that determination of hepatitis C genotype, as a key tool, is essential in controlling therapeutic regimen, improving local control programs and eventually producing an effective vaccine.

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The mechanistic (or mammalian) target of rapamycin (mTOR) is considered as a critical regulatory enzyme involved in essential signaling pathways affecting cell growth, cell proliferation, protein translation, regulation of cellular metabolism, and cytoskeletal structure. Also, mTOR signaling has crucial roles in cell homeostasis via processes such as autophagy. Autophagy prevents many pathogen infections and is involved on immunosurveillance and pathogenesis. Immune responses and autophagy are therefore key host responses and both are linked by complex mTOR regulatory mechanisms. In recent years, the mTOR pathway has been highlighted in different diseases such as diabetes, cancer, and infectious and parasitic diseases including leishmaniasis, toxoplasmosis, and malaria. The current review underlines the implications of mTOR signals and intricate networks on pathogen infections and the modulation of this master regulator by parasites. Parasitic infections are able to induce dynamic metabolic reprogramming leading to mTOR alterations in spite of many other ways impacting this regulatory network. Accordingly, the identification of parasite effects and interactions over such a complex modulation might reveal novel information regarding the biology of the abovementioned parasites and might allow the development of therapeutic strategies against parasitic diseases. In this sense, the effects of inhibiting the mTOR pathways are also considered in this context in the light of their potential for the prevention and treatment of parasitic diseases.

Introduction:The frequencies and functions of T stem cell memory (TSCM) subsets vary in autoimmune diseases. We evaluated the frequencies of CD4 + and CD8 + TSCM subsets as well as their PD-1 expression levels in patients with T1D. Methods: Blood samples were collected from new case (NC) (n = 15), and long-term (LT) (n = 15) groups and healthy controls (n = 15). Five subsets of T cells including TCM(CD4 + /CD8 + CCR7 + CD45RO + CD95 + ), TCM hi (CD4 + / CD8 + CCR7 + CD45RO hi CD95 + ), TEM(CD4 + /CD8 + CCR7 − CD45RO + CD95 + ), TSCM(CD4 + /CD8 + CCR7 + CD45RO − CD95 + ), and T naive (CD4 + / CD8 + CCR7 + CD45RO − CD95 − ) were detected by flow-cytometry. Results:The frequency of CD4 + TSCM was higher in NC patients than LT patients and controls (p < .0001 and p = .0086, respectively). A higher percentage of the CD8 + T naive cells was shown in NC patients as compared with LT and healthy individuals (p = .0003 and p = .0002, respectively). An increased level of PD-1 expression was observed on the CD4 + TCM and TCM hi cells in LT patients as compared with healthy controls (p = .0037 and p = .0145, respectively). Also, the higher PD-1 expression was observed on the CD8 + TCM and TCM hi in NC and LT patients as compared with controls (p = .0068 and p < .0001; p = .0012 and p = .0012, respectively). Conclusion:Considering TSCMs' capacities to generate all memory and effector T cells, our results may suggest a potential association between the increased frequencies of TSCMs and T1D progression.

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