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- Title
Dissociation of Autoaggression and Self-Superantigen Reactivity.
- Authors
Gonzalo, José Angel; de Alborán, Ignaclo M.; Kroemer, G.
- Abstract
Self-superantigens have been described as products of endogenous retroviruses of the mouse (`minor lymphocyte stimulating loci') that are capable of interacting without prior processing with conserved domains of TCR Vβ chains, causing the activation and deletion of most T cells expressing products of determined Vβ gene families [1-4]. The fact that superantigens activate a far higher percentage of T cells (1-20%) than conventional, peptidic antigens (<0.1 %) provides the methodological advantage that the degree of clonal deletion may be measured by the analysis of the TCR repertoire using appropriate anti-Vβ antibodies. Although much information on the spatio-temporal organization of repertoire-purging has been gathered by virtue of self-superantigens, serious doubts exist as to the possibility that such structures serve as pathogenetically relevant autoantigens. Thus, certain inbred mice spontaneously develop autoimmune diseases, although they bear T-cell repertoires that appear to be purged from self- superantigen-reactive Vβ products. In addition, therapeutic interventions targeted to Vβ gene products that are not specific for self-superantigens are successful in preventing disease development. The lack of correlation between superantigen- related Vβ deletions and autoimmune disease development is substantiated in further models of murine autoimmunity. Based on these observations, we formulate the hypothesis that self-superantigen-reactive T cells are not involved in the development of autoimmune diseases.
- Subjects
SUPERANTIGENS; LYMPHOCYTES; T cells; AUTOIMMUNE diseases; RETROVIRUSES; LABORATORY mice
- Publication
Scandinavian Journal of Immunology, 1993, Vol 37, Issue 1, p1
- ISSN
0300-9475
- Publication type
Editorial
- DOI
10.1111/j.1365-3083.1993.tb01657.x