Conclusions

In a genetically susceptible host, exogenous and hormonal factors influence the immune system at multiple levels, leading to numerous immunoregulatory abnormalities. The latter leads to generation of effector mechanisms of autoimmune pathology, including autoantibodies, immune complexes, autoreactive cells, and byproducts of immune activation, including lymphokines. T cells interact with B cells by cognate and noncognate means to help them produce autoantibodies. Autoantigens are revealed to the immune system because stressful stimuli such as UV light irradiation of keratinocytes (from exposure to sunlight) induce surface expression of previously hidden nuclear or cytoplasmic constituents. Immune complexes formed in excess amounts are cleared in decreased rates, resulting in increased serum levels and enhanced tissue deposition (Fig. 1.1).

Recent advances in scanning the human genome are expected to identify all genes involved in expression of the disease. When this is accomplished, we may be able to provide accurate genetic counseling and identify genes whose products are involved in the pathogenesis of the disease and the expression of pathology.

Hormonal

Autoantigen

Immune Complexes

Hormonal

Autoantigen

Immune Complexes

Increased Adhesion Molecule Expression

Fig. 1.1. Summary of the major cellular aberrations involved in the pathogenesis of lupus erythematosus (LE). Multiple genetic, environmental, and hormonal factors instigate a variety of cellular and cytokine abnormalities. These abnormalities lead to increased production of autoanti-bodies, which either directly or after forming complexes with autoantigens and activating complement deposit in tissues and initiate an inflammatory response. Immune complexes are formed in excessive amounts in patients with LE and are cleared at decreased rates because the numbers or the function of Fc and complement receptors are decreased.APC, antigen-presenting cells; autoAb, autoantibody; CR, complement receptor; FcR, Fc receptor; IFN, interferon; IL, inter-leukin; MHC, major histocompatibility complex; RES, reticuloendothelial system; UV, ultraviolet

Abnormal Signaling Increased Help Decreased Cytotoxicity Altered Cytokine Production decreased IFN-y, IL-2, IL-12 Increased IL-6, IL-10 Abnormal Gene Transcription

Increased Adhesion Molecule Expression

Fig. 1.1. Summary of the major cellular aberrations involved in the pathogenesis of lupus erythematosus (LE). Multiple genetic, environmental, and hormonal factors instigate a variety of cellular and cytokine abnormalities. These abnormalities lead to increased production of autoanti-bodies, which either directly or after forming complexes with autoantigens and activating complement deposit in tissues and initiate an inflammatory response. Immune complexes are formed in excessive amounts in patients with LE and are cleared at decreased rates because the numbers or the function of Fc and complement receptors are decreased.APC, antigen-presenting cells; autoAb, autoantibody; CR, complement receptor; FcR, Fc receptor; IFN, interferon; IL, inter-leukin; MHC, major histocompatibility complex; RES, reticuloendothelial system; UV, ultraviolet

Although better use of immunosuppressants and improved health care delivery have effectively decreased disease morbidity and mortality, there still is a long way to go before conquering this disease. Understanding the immunoregulatory abnormalities has helped in designing rational approaches to expand our therapeutic armamentarium. Biologic agents that can specifically reverse certain immune aberrations should further help patients with LE by improving survival and quality of life, and limiting adverse effects.

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