Viruses, cytokines, antigens, and autoimmunity

Roberto Gianani, Nora Sarvetnick

Research output: Contribution to journalReview articlepeer-review

80 Scopus citations

Abstract

To explain the pathogenesis of autoimmunity, we hypothesize that following an infection the immune response spreads to tissue-specific autoantigens in genetically predisposed individuals eventually determining progression to disease. Molecular mimicry between viral and self antigens could, in some instances, initiate autoimmunity. Local elicitation of inflammatory cytokines following infection probably plays a pivotal role in determining loss of functional tolerance to self autoantigens and the destructive activation of autoreactive cells. We also describe the potential role of interleukin 10, a powerful B-cell activator, in increasing the efficiency of epitope recognition, that could well be crucial to the progression toward disease.

Original languageEnglish (US)
Pages (from-to)2257-2259
Number of pages3
JournalProceedings of the National Academy of Sciences of the United States of America
Volume93
Issue number6
DOIs
StatePublished - Mar 19 1996

ASJC Scopus subject areas

  • General

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