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Reduced development of CD4-8-B220+ T cells but normal autoantibody production in lpr/lpr mice lacking major histocompatibility complex class I molecules

Ohteki, T.
Iwamoto, Masahiro
MacDonald, H. R.
Published in European Journal of Immunology. 1995, vol. 25, no. 1, p. 37-41
Abstract The lpr gene has recently been shown to encode a functional mutation in the Fas receptor, a molecule involved in transducing apoptotic signals. Mice homozygous for the lpr gene develop an autoimmune syndrome accompanied by massive accumulation of double-negative (DN) CD4-8-B220+ T cell receptor-alpha/beta+ cells. In order to investigate the origin of these DN T cells, we derived lpr/lpr mice lacking major histocompatibility complex (MHC) class I molecules by intercrossing them with beta 2-microglobulin (beta 2m)-deficient mice. Interestingly, these lpr beta 2m-/- mice develop 13-fold fewer DNT cells in lymph nodes as compared to lpr/lpr wild-type (lprWT) mice. Analysis of anti-DNA antibodies and rheumatoid factor in serum demonstrates that lpr beta 2m-/- mice produce comparable levels of autoantibodies to lprWT mice. Collectively our data indicate that MHC class I molecules control the development of DN T cells but not autoantibody production in lpr/lpr mice and support the hypothesis that the majority of DN T cells may be derived from cells of the CD8 lineage.
Keywords AnimalsAntigens, CD45Antigens, Surface/immunologyAutoantibodies/ biosynthesisCell Differentiation/immunologyFemaleFlow CytometryHistocompatibility Antigens Class I/ immunologyImmunophenotypingMiceMice, Mutant StrainsT-Lymphocytes/ immunologybeta 2-Microglobulin/deficiency/immunology
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PMID: 7531148
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