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Functional analysis of T cell subsets from mice bearing the lpr gene

Davignon, J. L.
Budd, R. C.
Ceredig, R.
Piguet, P. F.
MacDonald, H. R.
Cerottini, J. C.
Published in Journal of Immunology. 1985, vol. 135, no. 4, p. 2423-2428
Abstract The autosomal recessive lpr (lymphoproliferation) gene is responsible for a thymus-dependent massive lymphoproliferation associated with the development of lupus-like autoimmune disease. Phenotypic analysis of adult lpr/lpr lymph nodes has demonstrated accumulation of a dull Lyt-1+, Thy-1+ population that expresses neither Lyt-2 nor L3T4 antigens. With the use of a depletion method based on complement-mediated lysis with an anti-Lyt-2 monoclonal antibody (31 M) and a new anti-L3T4 monoclonal antibody (RL 172.4), we have purified the Lyt-2- L3T4- subset from lymph nodes or spleens of C57BL/6-lpr/lpr mice and determined whether they are immunologically functional in vitro. Production of neither interleukin 2 nor interferon-gamma was detected by the double-negative subset after stimulation with concanavalin A and/or phorbol myristate acetate. The frequencies of allospecific cytotoxic T lymphocyte (CTL) precursors and lectin-induced antigen-nonspecific CTL precursors were diminished to almost undetectable levels, whereas the Lyt-2+ population from lpr/lpr mice had CTL-precursor frequencies comparable with that of +/+ mice. These results show that the major cell subset of adult lpr/lpr lymph nodes or spleens is composed of lymphocytes with markedly limited potential for lymphokine production or antigenic stimulation.
Keywords AnimalsAntigens, LyAntigens, Surface/analysisCell SeparationConcanavalin A/pharmacologyCytotoxicity, ImmunologicFemaleFlow CytometryGenes, RecessiveInterferon-gamma/biosynthesisInterleukin-2/biosynthesisIsoantigens/immunologyLymphocyte ActivationMaleMiceMice, Inbred C3HMice, Inbred C57BLMice, Inbred DBAMice, Mutant Strains/ immunologyPhenotypeT-Lymphocytes/ classification/immunologyT-Lymphocytes, Cytotoxic/immunology
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Other version: http://www.jimmunol.org/cgi/reprint/135/4/2423.pdf
PMID: 3928747
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