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The failure of immunological tolerance to self‐antigens plays a fundamental role in the pathogenesis of systemic lupus erythematosus (SLE). PD‐1 is an inhibitory receptor for regulating the immune system and preventing development of autoimmune disorders. This study aimed to determine the role of four single‐nucleotide polymorphisms (SNPs) within programmed cell death 1 (PDCD1 or PD‐1) gene and haplotypes defined by these SNPs in susceptibility to SLE in the Iranian population. Blood samples were obtained from 253 SLE and 564 healthy subjects. Red blood cells were lysed and genomic DNAs were extracted using salting‐out method. Genotype determinations of PD1.1, PD1.3, PD1.5 and PD1.9 SNPs were performed by polymerase chain reaction–restriction fragment length polymorphism (PCR‐RFLP), and 12 haplotypes were constructed by PDCD1 SNPs. Our results showed significant differences in PD1.5 genotype frequencies between patient and control groups (p <.001). The frequencies of PD1.5 C/C, C/T and T/T genotypes versus other genotypes in SLE patients significantly differed from healthy subjects (p <.001, p =.001 and p =.002, respectively). Allelic analysis indicated a significant association between the frequency of PD1.5C allele and development of SLE in our population (odds ratio [OR] = 1.91, 95% confidence interval [CI] = 1.51–2.42, p <.001). At the haplotype level, GGCC, GACT and GGCT haplotypes were significantly different between SLE and control groups (OR = 2.14, 95% CI = 1.73–2.66, p <.001; OR = 9.76, 95% CI = 4.47–21.3, p <.001; and OR = 0.32, 95% CI = 0.24–0.42, p <.001, respectively). Based on these findings, PD1.5 SNP and some haplotypes of PDCD1 contribute to SLE risk in the Iranian population. [ABSTRACT FROM AUTHOR]

Background: Laboratory health care workers (HCWs) may become infected through their occupation with blood-borne pathogens. The aims of this study were determining the seroprevalence of hepatitis B virus (HBV) and the protection offered by HBV vaccine in medical laboratory HCWs. Materials and Methods: A descriptive cross-sectional study was carried out on 203 employers of clinical laboratories. Participant data were obtained through a questionnaire, and the level of antigens and antibodies were measured by enzyme-linked immunosorbent assay (ELISA). Results: All of the subjects were negative for HBV infection. Forty-seven (23.2%) were not immune, 126 (62.0%) were relatively immune, and 30 (14.8%) were highly immune. Conclusion: Hepatitis B infection is infrequent in laboratory HCWs in Isfahan. [ABSTRACT FROM AUTHOR]

Schizophrenia (SZ) is a severe psychiatric disorder associated with a dysregulation of the immune system. Immune-related genes and environmental factors including stress, food, infections, and microbiota, alter the immune system's homeostasis and play a role in SZ pathogenesis. The most distinctive feature in the pathophysiology of the disease is a shift in the T helper 1(Th1)/Th2 balance toward Th2 dominance in the immune system. Also, microglial and Th17 cell activation cause inflammatory responses in the central nervous system (CNS). Antibodies play a role in the pathophysiology of SZ and give more evidence of a link between humoral immune reactivity and the disease. Accordingly, an imbalance in cytokine activities and neuroinfl ammation has been considered the main contributor to the pathogenesis of the SZ. Overall, the deregulation of the immune system caused by genetic, environmental, and neurochemical effects may all play a role in the etiology of SZ. This review summarized the etiological factors for SZ and discussed the role of immune responses and their interaction with genetic and environmental factors in SZ pathogenesis., Competing Interests: None., (Copyright© 2023, Galen Medical Journal.)