OVA G4 peptide

The alloreactivity of T cells is thought to be based on the cross-reactive recognition of allogeneic major histocompatibility complex (MHC) molecules which have bound peptides derived from self antigens or, in the case of cultured T cells, from serum components. While studying the processing requirements of conalbumin (CA) that is recognized by D10.G4.1 T cells in combination with I-Ak molecules we also analysed the cross-reactive stimulation of clone D10.G4.1 T cells by allogeneic, I-Ab expressing stimulator cells which is shown here to be CD4 dependent. In order to distinguish between an endogenous or exogenous origin of a peptide that is presumably co-recognized with I-Ab different types of stimulatory/antigen-presenting cells (APC) were treated with drugs that are known to influence the processing and/or presentation of antigens. It was found that the alloreactive response of D10.G4.1 cells was abolished if the APC were treated with brefeldin A or inhibitors of protein biosynthesis. Under the same conditions neither the CA-specific response of D10.G4.1 cells nor the activation of control T cells by ovalbumin (OVA) or insulin was affected. On the other hand, the use of lysosomotropic agents or inhibitors of glycoprotein trimming had no influence on the ability of the APC to induce the alloresponse of D10.G4.1 cells, whilst the presentation of CA and other protein antigens by the APC was prevented. In addition, treatment of APC with pronase to remove surface MHC molecules or acidic buffer to remove peptides from the binding groove of MHC class II molecules at the surface of APC strongly diminished their ability to induce an alloresponse. However, this capacity was restored by incubating the APC for 2 hr in serum-free medium. These data indicate that the alloreactive response of D10.G4.1 cells is based on the recognition of newly synthesized endogenous peptide(s) in combination with I-Ab.

Bronchial asthma (BA) is a heterogeneous allergic respiratory disease with diverse inflammatory symptoms, pathology, and responses to treatment. Thyme is a natural product which is consisted of multiple phenolic compounds of therapeutic significance for treatment of cough and bronchitis. This study evaluated the efficacy of thyme oil against ovalbumin (OVA)-induced BA in an experimental rabbit model. Forty male rabbits were divided into four equal groups [control group (G1), OVA (G2), thyme oil (G3), and OVA plus thyme oil (G4)]. Animals were treated for 30 days, and clinical, histopathological (HP), histochemical (HC), immunohistochemical (IHC), morphometric, biochemical and flow cytometry methods were performed, followed by statistical analysis. All used methods revealed normal structure of the lung tissues in rabbits of G1 and G3. In contrast, the clinical examination of G2 rabbits revealed an obvious increase in the respiratory rate, sneezing and wheezing, whereas the HP, HC and IHC techniques exhibited substantial inflammatory changes in the peribronchio-vascular lung tissues with thinning, degeneration, apoptosis (using the TUNEL assay), necrosis, and shedding of the airway epithelium. Furthermore, the morphometric results confirmed significant increases in the numbers of inflammatory cells, goblet cells, eosinophils and apoptotic cells from (12, 0, 2, 2 cells) to (34,10, 16, 18 cells) respectively, as well as the area percentage of collagen fiber deposition and immunoexpression of eotaxin-1/10 high power fields. Additionally, the biochemical results revealed significant increases in the serum levels of TSLP, IL-4, IL-5, IL-9, IL-13, IgE and eotaxin-1 cytokines from (140, 40, 15, 38, 120, 100, 48) pg./ml to (360, 270, 130, 85, 365, 398, 110) pg./ml respectively, while analysis of ROS by flow cytometry revealed remarkable oxidative stress effects in G2 rabbits. On the other hand, treatment of rabbits with thyme oil in G4 substantially alleviated all OVA-induced alterations. Overall, our findings indicate for the first time that thyme oil can ameliorate OVA-induced BA via its immunomodulatory, anti-inflammatory, antiapoptotic, and antioxidant effects on the lung tissues of rabbits.

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.