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Primary Sjögren's Syndrome After Infectious Mononucleosis

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Grant support: Drs. Whittingham and Mackay received a grant from the National Health and Medical Research Council of Australia.

▸Requests for reprints should be addressed to Senga Whittingham, M.D., Ph.D.; The Walter and Eliza Hall Institute of Medical Research, Post Office Royal Melbourne Hospital; Victoria 3050, Australia.

Victoria, Australia

©1985 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1985;102(4):490-493. doi:10.7326/0003-4819-102-4-490
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A healthy young woman developed primary Sjogren's syndrome after protracted infectious mononucleosis. The diagnosis of primary Sjögren's syndrome was supported by histologic evidence of sialadenitis in labial salivary glands, rheumatoid factor, hypergammaglobulinemia, the HLA-B8 phenotype, and a high titer antibody to the La (SS-B) nucleoprotein that co-precipitated the small ribonucleic acids encoded by Epstein-Barr virus, EBER 1 and EBER 2, as well as "host" RNA. There was strong humoral immunity to the Epstein-Barr nuclear and capsid antigens, but weak T-lymphocyte-mediated cytotoxicity to Epstein-Barr-transformed lymphoblasts, anergy to antigens used to elicit delayed-type hypersensitivity, and a low T-helper/T-suppressor cell ratio. The series of events initiated by infectious mononucleosis was attributed to a genetic defect in the immune response. Association of viral RNA with the La nucleoprotein resulted in a break in immunologic tolerance via a T-cell bypass effect with induction of anti-La (SS-B) by polyclonally activated B lymphocytes leading to autoimmune sialadenitis.





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