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Editorials |

Excitement—and Confusion—about HLA and Rheumatoid Arthritis

Edward D. Harris Jr., MD
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Stanford University School of Medicine, Palo Alto, CA 94304-1808 Requests for Reprints: Edward D. Harris Jr., MD, Stanford University School of Medicine, 1000 Welch Road, Suite 203, Palo Alto, CA 94304-1808.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1995;123(3):232-233. doi:10.7326/0003-4819-123-3-199508010-00012
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Rheumatoid arthritis has successfully resisted the efforts of many investigators to find a specific cause of the disease or a single genetic basis for risk. Vigorous debate continues about whether a retrovirus from the environment, an autoantigen from a patient's connective tissues or plasma, or a cross-reactive immune response between host tissues and a superantigen (for example, bacterial heat shock proteins) triggers this disease. Except for a person's recognized high risk for developing rheumatoid arthritis when she or he has an identical twin with the disease [1], there was little evidence for a genetic predisposition until Astorga and Williams [2] reported in 1969 that in 14 of 22 different patients with rheumatoid arthritis, lymphocytes mixed in cultures did not activate each other. These data, which in retrospect implied identical cell membrane antigens in the cells of different patients, attracted little attention until Stastny [3] found that in a cohort of white persons, 68% of patients with rheumatoid arthritis but only 12% of controls shared type Dw4 in the major histocompatibility complex (MHC).

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