SLE is a prototype of systemic autoimmune disease of unknown cause, multiple organ involvement (skin rash, arthritis, pleuritis, pericarditis, nephritis, etc.,), predilection for young women particularly in the child-bearing years, and multi-factorial pathogenesis (see Immunopathology/SLE).

SLE, a systemic connective tissue disease in its pathology, is characterized by the presence of anti-nuclear autoantibodies (ANA), a generic group of serum, mainly IgG, autoantibodies that react by indirect immunofluorescence test with acetone-fixed cell nuclei from a wide range of tissues and animal species (thus lacking tissue and species specificity). ANA in SLE may also react specifically with isolated and characterized nuclear antigens, such as deoxyribonucleoprotein, DNA in double (ds) and single (ss) strand configuration, histones (from chromatin), non-histone proteins such as nuclear and nucleolar ribonucleoproteins (RNPs), Sm antigen, etc. None of these reactivities has absolute specificity for any disease entity. The highest specificity for active SLE is apparently given by anti-dsDNA autoantibodies which are rarely found at significant levels in other diseases.

DNA-antiDNA autoantibodies contribute to the pathogenesis of immune complex and complement mediated tissue injury and inflammation in SLE expressed as nephritis, vasculitis, and serositis. Autoantibodies are also produced in some lupus patients against platelets, erythrocytes, T-cells or other self components, and contribute to autoantibody initiated cell injury resulting in thrombocytopenia, hemolytic anemia, lymphopenia, etc.

CD20 B-lymphocytes are precursors of plasma cellswhich are terminally differentiated from B-lymphocytes to produce immunoglobulins, antibodies, and autoantibodies but do not express the CD20 B-lymphocyte-specific cell membrane surface antigen.

The central pathogenic importance of autoimmune B-lymphocytes is now well recognized and provides the rationale for targeting B-lymphocytes in autoimmune diseases (Dorner, T., J Rheumatol Suppl. 77, 3-11, 2006). This insight into a new molecular target has led to the development of CD20-B cell specific monoclonal antibody (rituxamab, Rituxan) for evaluation in the therapy of non-Hodgkin's CD20 lymphoma, rheumatoid arthritis, , and systemic lupus erythematosus.

Mycophenolate mofetil (MMF) is an immunosuppressive agent, an inhibitor of the enzyme inosine monophosphate dehydrogenase required for purine synthesis, especially by activated lymphocytes, and MMF has been used for more than a decade in the organ transplantation field. Recent anecdotal reports and controlled preliminary trials have described the benefits and need for further evaluation of MMF in the treatment of lupus nephritis, a serious and potentially life-threatening manifestation of SLE (Dooley, M.A., Lupus 15, 179-82, 2006; McCune, W.J., N Engl J Med 353, 2282-2284, 2005).

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