Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rheumatoid arthritis and systemic lupus erythematosus are rheumatic diseases characterized by excessive immunoreactivity. Exaggerated immunity is manifested as auto-antibody production and aberrant cell-mediated reactions directed against autologous tissue. Although the mechanisms and site for abnormal immune responses are not completely understood, risk factors that predispose an individual to develop rheumatoid arthritis or systemic lupus erythematosus can be defined. Genetic factors, especially HLA genes, play an important role in rendering a host susceptible to the sequelae of immunologically mediated diseases. Modern technology, such as T-cell cloning, can be used to dissect polymorphic HLA determinants involved in the genetic susceptibility for rheumatoid arthritis and systemic lupus erythematosus. Mapping of disease-associated determinants in rheumatoid arthritis patients suggests that polymorphic sites within the third hypervariable region of the HLA-DR beta 1-chain are functionally involved in the initiation and perpetuation of the disease. These HLA-determinants function to mediate the contact between the HLA- and the T-cell receptor molecules. In systemic lupus erythematosus patients, the role of disease associated molecules appears to be distinct; genetic susceptibility is correlated to patterns of auto-antibody productions. Immunogenetic studies may provide diagnostic tools to subset patients with rheumatoid arthritis and systemic lupus erythematosus and develop prognostic markers to tailor immunomodulatory therapy. Both diseases are characterized by high levels of morbidity and mortality, but can now be mitigated by the careful and judicious use of immunosuppressives.
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PMID:Diagnostic, prognostic and therapeutic aspects of systemic lupus erythematosus and rheumatoid arthritis. 219 90

Z39Ig is a recently-identified gene with immunoglobulin-like domains whose function is unknown. We examined expression of Z39Ig in 1432 human cDNA libraries, and found it primarily in synovium of patients with rheumatoid arthritis, in placenta, and in lung. We analyzed its co-expression pattern using the Guilt-by-Association (GBA) algorithm, and found that it is most similar in expression to early genes in the classical complement system (C1qA, C1qB, C1qC, C1r, and C1 inhibitor), MHC class II genes (HLA-DR alpha, HLA-DR beta 1, and HLA-DP alpha 1), Fc receptors (Fc gamma RIIa and Fc epsilon R1), lysosomal protein (LAPTm5), tissue transglutaminase, and macrophage receptors (MARCO and CD163/M130). The sequence and expression data suggest that Z39Ig is a cell surface receptor, expressed in activated macrophages, and linked with the classical complement system, most likely in phagocytosis preceding antigen presentation. Knowledge of this gene may contribute to better understanding of the role of complement and activated macrophages in rheumatoid arthritis and systemic lupus.
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PMID:Z39Ig is co-expressed with activated macrophage genes. 1199 8