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Major histocompatibility complex genes in systemic lupus erythematosus, Sjögren's syndrome, and polymyositis.

Abstract
Current concepts about the roles of human leukocyte antigen (HLA) and complement genes in predisposing to connective tissue diseases are reviewed. Precise localization of disease conferring alleles and epitopes is confounded by two major phenomena: (1) clinical and serologic heterogeneity of the diseases and associations of several different HLA alleles with different and often overlapping autoantibody responses; and (2) linkage disequilibrium of many potentially relevant gene loci located on the disease-associated HLA haplotypes. Using molecular genetic tools in serologically homogeneous patient populations, and across racial lines, the Ro (SS-A) and la (SS-B) autoantibody responses in systemic lupus erythematosus and Sjögren's syndrome appear to associate most strongly with HLA-DQ alleles, whereas the anti-Jo-1 autoantibody in myositis correlates best with HLA-DRw52. A gene deletion of C4A within HLA predisposes to systemic lupus erythematosus in both white and black patients.
AuthorsF C Arnett, R Goldstein, M Duvic, J D Reveille
JournalThe American journal of medicine (Am J Med) Vol. 85 Issue 6A Pg. 38-41 (Dec 23 1988) ISSN: 0002-9343 [Print] United States
PMID2462349 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Antibodies, Antinuclear
  • Epitopes
  • HLA Antigens
Topics
  • Alleles
  • Antibodies, Antinuclear (analysis)
  • Epitopes (genetics)
  • Genetic Linkage
  • HLA Antigens (genetics)
  • Humans
  • Lupus Erythematosus, Systemic (genetics, immunology)
  • Major Histocompatibility Complex
  • Myositis (genetics, immunology)
  • Sjogren's Syndrome (genetics, immunology)

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