| First Author | Wen L | Year | 1994 |
| Journal | Nature | Volume | 369 |
| Issue | 6482 | Pages | 654-8 |
| PubMed ID | 8208291 | Mgi Jnum | J:111129 |
| Mgi Id | MGI:3653069 | Doi | 10.1038/369654a0 |
| Citation | Wen L, et al. (1994) Immunoglobulin synthesis and generalized autoimmunity in mice congenitally deficient in alpha beta(+) T cells. Nature 369(6482):654-8 |
| abstractText | Through cognate B-cell-T-cell interactions and provision of cytokines, CD4+ T-cell antigen receptor (TCR) alpha beta+ T cells regulate immunoglobulin isotype synthesis. Murine IgG1 and IgE secretion is therefore substantially T-cell-dependent, whereas IgM and IgG3 secretion is not. Here we report that in the absence of alpha beta 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+ alpha beta T cells. This phenotype is not evident in mice or humans that are congenitally deficient in specific alpha beta T-cell functions, but bears comparison with B-cell hyperactivity and autoimmunity in transplant rejection and in immunodeficiencies such as AIDS. |
