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.
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Wen, L., Roberts, S., Viney, J. et al. Immunoglobulin synthesis and generalized autoimmunity in mice congenitally deficient in αβ(+) T cells. Nature 369, 654–658 (1994). https://doi.org/10.1038/369654a0
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DOI: https://doi.org/10.1038/369654a0
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