Analysis of CD69 and CD28 activating and CTLA-4 regulator molecules of t CD4 cells and expression of Treg CD4+CD25+FoxP3+ cells on peripheral blood and spleen of mice with systemic lupus erythematosus (SLE) pristane-induced

• Grant number: 14/09627-9
• Support Opportunities: Regular Research Grants
• Start date: August 01, 2014
• End date: July 31, 2016
• Field of knowledge: Biological Sciences - Immunology - Cellular Immunology
• Principal Investigator: Claudia Goldenstein Schainberg
• Grantee: Claudia Goldenstein Schainberg
• Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Associated researchers: Francisco Garcia Soriano ; Suzana Beatriz Verissimo de Mello

Abstract

Systemic Lupus Erythematosus (SLE) is an auto immune disease that affects 1 in every 1.700 woman in Brazil. It has a complex etiology involving environmental, genetic and hormonal factors. It is multisystemic and characterized by the loss of immunologic auto-tolerance with activation e proliferation of self-reactive T cells and production of inflammatory and auto-antibody mediators. The primary receptor of activation CD69 and co-stimulator molecule CD28 are essential to maintain the activation and proliferation of self-reactive T CD4 cells. In contrast, CTLA-4 works as a regulator for these cells, inhibiting their activation and proliferation. The activity of self-reactive T CD4 cells is also controlled by T suppressors/regulator cells (Treg) CD4+CD25+FoxP3+. In patients with SLE, CD69 expression is increased and Treg is reduced, however the exact part of these immunologic anomalies still need further studies. Experimental models that developed syndromes similar to the human pathology are important. The administration of pristane in Balb/c mice induces inflammatory responses with auto-antibody production, reproducing serological, histopathological and clinical factors of human SLE. However, is important to highlight that the data currently available do not describe nor explain all of the immunological anomalies observed in this pathology. Thus, in order to comprehend the beginning and the perpetuation of the imuno homeostatic unbalance in pristane-induced SLE, the objectives is to evaluate, on peritoneal wash, blood and spleen of these mice, the expression of: 1) cells activated by the expression of CD69 and CD28 receptors; and 2) Treg cells, suggesting this murine model may knowledge concerning immunological abnormalities found in SLE, contributing for the comprehension and understanding of the human pathology. (AU)