Immunoglobulin synthesis and generalized autoimmunity in mice congenitally deficient in αβ(+) T cells
Open Access
- 1 June 1994
- journal article
- letter
- Published by Springer Science and Business Media LLC in Nature
- Vol. 369 (6482), 654-658
- https://doi.org/10.1038/369654a0
Abstract
THROUGH cognate B-cell–T-cell interactions and provision of cytokines, CD4+ T-cell antigen receptor (TCR) αβ+ T cells regulate immunoglobulin isotype synthesis1. Murine IgGl and IgE secretion is therefore substantially T-cell-dependent, whereas IgM and IgG3 secretion is not2, 3. Here we report that in the absence of αβ T cells, B cells expand, differentiate and secrete copious amounts of antibodies of ‘T-dependent’ isotypes. Moreover, the antibodies are reactive towards self-antigens, as in patients with systemic lupus erythematosus, so autoantibodies of ‘ T-dependent type can develop without the help of CD4+ αβ T cells. This phenotype is not evident in mice or humans that are congenitally deficient in specific αβ T-cell functions, but bears comparison with B-cell hyperactivity and autoimmunity in transplant rejection and in immunodeficiencies such as AIDS4, 5.Keywords
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