Investigation of the relationship of tissue-resident γδ T cells and IL-17 gene expression with the pathogenesis of autoimmune hepatitis.

Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease. Elevated serum immunoglobulin G (IgG) levels, autoantibodies, and histopathological interface hepatitis are the hallmarks of AIH. Autoantibodies and pathological findings, clinical and biochemical features, typical immunoglobulin levels, and exclusion of other diseases are used to diagnose the condition. Gamma-delta (γδ) T cells are a unique population of unconventional T cells with γ and δ glycoprotein chains. γδ T cells have been shown to play a crucial role in autoimmune diseases by producing interleukin (IL)-17. However, its role in AIH remains to be further elucidated. In this study, we aimed to examine the role of γδ T cells and IL-17 in the pathogenesis of AIH, by working on biopsy samples. Paraffin blocks of 18 patients with type 1 AIH and 18 control liver tissues were analyzed. qRT-PCR assessed IL-17 gene expression. Immunofluorescence double staining of CD3+TCRγδ+ was performed to reveal tissue-resident γδ T cells' role in AIH. When comparing AIH to the control, there was a substantial increase in the ratio of CD3+TCRγδ+ cells in total inflammatory cells (p = 0.01). IL-17 gene expression was lowered in AIH when compared to the control (p = 0.01). This study provides evidence for the involvement of γδ T cells and IL-17 in the pathogenesis of AIH. The ratio of γδ T cells and IL-17 gene expression showed a significant difference in AIH suggesting a potential role for γδ T cells in driving liver inflammation in A fIH.

Propolis protects ovarian follicular reserve and maintains the ovary against polycystic ovary syndrome (PCOS) by attenuating degeneration of zona pellucida and fibrous tissue.

To examine the effects of 50 mg/kg and 150 mg/kg of propolis on ovarian folliculogenesis, p53 expression, and serum luteinising hormone (LH) and progesterone (P) levels in polycystic ovary syndrome (PCOS) modeled rats. Twenty-four Wistar female rats were divided into 4 experimental groups: Group 1 (G1, Control), Group 2 (G2, PCOS), Group 3 (G3, PCOS + 50 mg/kg propolis), and Group 4 (G4, PCOS + 150 mg/kg propolis). The PCOS model was induced via the administration of letrozole for 21 days. After 21 days, G3 and G4 received propolis (50 mg/kg or 150 mg/kg) by oral gavage for 10 days. Daily oestrous cycles were assessed to monitor PCOS formation. Histological examinations were carried out using haematoxylin and eosin (H&E) and Masson Trichrome (MT) staining. Ovarian follicles and corpus luteum (CL) structures were investigated. P and LH serum levels were determined by ELISA. A significant increase was observed in the number of cystic follicles in G2 compared to G1 (p < 0.001). Treatment with 50 mg/kg of propolis significantly ameliorated the elevated number of cystic and primary follicles seen in G2 (p < 0.001). Furthermore, G2 demonstrated a significant decrease in the number of CL structures (p < 0.05). Serum LH levels were significantly higher in G4 compared to both G1 and G2 (p < 0.01). No significant change was observed in circulating P levels. No p53 immunoreactivity was observed in any group. Low concentrations of propolis cannot completely improve the hormone profile and p53 expression associated with PCOS; however, these concentrations can control ovarian follicular cell architecture.