These data suggest that increase in mtDNAcn and oxidative DNA damage may be involved in the pathogenesis of vitiligo.

These data suggest additional implications for the role of Th1/Th2 balance in the immunopathogenesis of vitiligo.

BackgroundPsoriasis is a chronic inflammatory disorder, characterized by increased keratinocyte proliferation due to abnormal differentiation of basal keratinocytes. The etiology of the disease is unclear, and according to the survey results, it is hypothesized that a combination of genetic and environmental factors prompts an abnormal immune response in patients with psoriasis. CD4+ Th cells play a multifaceted role in both immune defense and pathogenesis of certain diseases such as psoriasis. Nonetheless, the exact contribution of different subpopulations of Th cells in psoriasis is still not clear. ObjectiveThe aim of present study was to determine the mRNA expression level of RORC as potential inducer of Th17 cell differentiation and expression pattern of Th17-signature cytokines (IL-17A and IL-22).MethodsTwenty patients with psoriasis and twenty-one healthy subjects were included in the study. Peripheral blood mononuclear cells (PBMCs) were separated and expression of three genes were determined by quantitative real-time reverse transcriptase PCR (qRT-PCR). Plasma levels of IL-17 and IL-22 were also evaluated by ELISA.ResultsRORC, IL-17A and IL-22 gene expression was significantly higher in patients with psoriasis compared with healthy controls (P<0.05). In addition, a marked increase in plasma IL-17A and IL-22 levels was observed in patient group compared to controls (P<0.001).Study limitationssmall number of patients.ConclusionThese data suggest that Th17 response may contribute to the pathogenesis of psoriasis.

The hepatitis C virus infection represents an important public health problem and is associated with various hepatic and extrahepatic manifestations. Symptoms outside of the liver can occur in multiple organ systems, including hematologic, renal, dermatologic, endocrine, and rheumatologic systems. Among these different organ systems, special attention has focused on the endocrine system because it affects almost every organ in the body. Among the endocrine disorders, thyroid problems are the most common and the thyroid is one of the principal target organs for extrahepatic manifestations in HCV infected patients. In addition, research data suggest that interferon treatment may be associated with immune-mediated thyroid lesions. However, case reports suggest that the response of thyroid extrahepatic manifestations to interferon in patients with chronic HCV is greatly different. The objective of this study was to summarize currently available data on thyroid conditions associated with chronic HCV infection. Moreover, we investigate the incidence of the development of immune mediated thyroid disorders during interferon therapy in these patients.

Background/Aims: Dysregulation of T cell response is thought to play an important role in the immunopathogenesis of autoimmune hepatitis. However, no consensus has yet been reached regarding the implications of a distinct T cell subset in the pathogenesis of this progressive liver disease. Therefore, T-bet and GATA-3 expression was examined in patients with autoimmune hepatitis (AIH) and in healthy controls. Moreover, the profile of Th1 (IFN-γ) and Th2 (IL-4) cytokine gene expression was analyzed. Materials and Methods: Levels of mRNA transcripts were measured in peripheral blood mononuclear cells (PBMCs) using a two-step reverse transcription quantitative real-time polymerase chain reaction with SYBR Green. Results: T-bet and IFN-γ mRNA expression was significantly higher in AIH patients compared to healthy controls (p<0.05), whereas no differences were observed for either GATA-3 or IL-4 mRNA expression (p>0.05). Conclusion: Alterations in the Th1/Th2 cell balance may be responsible for both disease progression and the resulting complications.