Immunoglobulin synthesis and generalized autoimmunity in mice congenitally deficient in alpha beta(+) T cells

Nature. 1994 Jun 23;369(6482):654-8. doi: 10.1038/369654a0.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Autoantibodies / biosynthesis
  • Autoantibodies / immunology
  • Autoimmunity / immunology*
  • B-Lymphocytes / immunology*
  • Cell Differentiation
  • Humans
  • Immunoglobulin E / biosynthesis
  • Immunoglobulin G / biosynthesis
  • Immunoglobulin Isotypes / biosynthesis*
  • Immunologic Deficiency Syndromes / congenital
  • Immunologic Deficiency Syndromes / immunology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Receptors, Antigen, T-Cell, alpha-beta
  • Spleen / cytology
  • T-Lymphocytes / immunology*


  • Autoantibodies
  • Immunoglobulin G
  • Immunoglobulin Isotypes
  • Receptors, Antigen, T-Cell, alpha-beta
  • Immunoglobulin E