Analysis of activator and regulatory molecules of CD4+ T cells and CD4+CD25+ Treg cells in mice with Systemic Lupus Erythematosus (SLE) pristane-induced

Abstract

Systemic Lupus Erythematosus is an autoimmune disease that affects about 80,000 people in Brazil. It has a complex etiology involving environmental, genetic and hormonal factors. It is a multisystemic, can affect multiple organs, characterized by loss of immunologic tolerance with self-production and expansion of autoreactive T cells and production of inflammatory mediators and autoantibodies. The cellular receptors CD69 and CD28 are essential for maintaining the activation and proliferation of self-reactive CD4 T cells because they increase the production of IL-2. In contrast, the CTLA-4 is a negative regulator of CD4 T cells, inhibiting their activation and proliferation. The activity of self-reactive CD4 T cells is also controlled by suppressor / regulatory CD4+ CD25+ T cells (Treg). The expression of CD69 and CD28 on CD4+ CD25+ T cells is important for the maintenance of their suppressive/regulator activity and CTLA-4 is essential to regulate signal transduction and differentiation of these cells. Because the heterogeneity of the expression of lupus in the population, experimental studies that develop pathology similar to human syndromes are important. The administration of pristane in BALB/c mice induces inflammatory responses with production of autoantibodies, reproducing many factors serological, histopathological and clinical features of human lupus. The melanocyte stimulating hormone (MSH) has anti-inflammatory effect capable of inhibiting the activation and proliferation of CD4 T cells. Thus, the objective is to evaluate the expression of activating molecules CD69 and CD28 and the regulatory molecule CTLA-4 in CD4 T cells and CD4+ CD25+ Treg cells from peripheral blood of BALB/c mice with pristane-induced SLE. The evaluation before and after treatment with alpha-MSH intents to help the comprehension of molecular and cellular events of abnormal SLE. (AU)