CD38 involvement in autoimmune disease using a murine model for systemic lupus erythematosus (148.13)

Abstract

Abstract Mouse models contribute in our understanding of human diseases. By this way, several strains of systemic lupus erythematosus (SLE)-prone mice including New Zealand Black (NZB), F1 hybrids of NZB x New Zealand White (NZW) (B/W F1), MRL/Mp-lpr/lpr (MRL/lpr), and BXSB mice are important in the research of the autoimmune diseases. Several genes and signaling pathways molecules have been related with SLE pathologies such as: Lyn, CD22, SHP-1 or the sle1, sle2 and sle3 congenic models. CD38 is a transmembrane receptor able to induce activation, proliferation, and survival of human and mouse lymphocytes; this molecule is expressed along the B cell ontogeny, in addition, CD38 is an ectoenzyme involved cell adhesion and is used as a disease marker for leukemia and myeloma, also is a dependable negative prognostic marker for chronic lymphocytic leukemia (CLL). The function of CD38 in autoimmunity has been proposed in human but there are not reports that clear the authentic role of this molecule in SLE. To study the implication of CD38 in the SLE pathogenesis we compare the proteinuria, serum ANA and anti-dsDNA antibody production, body-weight, nephritis and mortality in the CD38-deficient compared to the wild type (WT) mice. Subsequently, we expect that the pathologic manifestations of nephritis appear significantly earlier in the WT mouse as well survival rate changes.