Autoimmune Disease Process

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown etiology. SLE is characterized by the involvement of multiple organ systems and the production of autoantibodies directed against nuclear components, including ssDNA, ds-DNA and histones [1-2], The hallmark of autoimmunity is the activation and proliferation of lymphocytes directed against self-antigen. Abnormalities in lymphoid cell function include: (i) changes in the ratio of T-cell subset population; (ii) increased T-helper and decreased T-suppressor functions; (iii) restricted usage of T-cell receptor genes; (iv) defect in programmed T-cell death mechanisms, (v) increased population of active T cells; (vi) increased expansion of B cells leading to the production of autoantibodies; and (vii) abnormalities in the signal transduction pathway in lymphocytes. Defect in the signal transduction cascade mechanisms in lymphocytes from SLE patients have been shown to result in the aberrant expression of many genes and some of which encode DNA sequence specific transcription factors [1], These in turn may regulate the transcription of genes contributing towards disease process.

In this chapter, we provide a brief overview of the ETS gene family (see recent reviews [3-7] for additional information and references). We discuss the expression pattern of ETS1, ETS2 and ERGB/FLI1 genes in lymphocytes from SLE patients and the possible role of ERGB/FLI1 transcription factor in the autoimmune disease process.

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