Regulation of antibody isotype secretion by subsets of antigen-specific helper T cells

Nature. 1988 Jul 21;334(6179):255-8. doi: 10.1038/334255a0.


The regulation of the subclass of immunoglobulin secreted by B cells has been studied in vitro in polyclonal systems using mitogens, such as lipopolysaccharide (LPS), to bypass the requirement for cognate interaction between antigen-specific T and B cells. In these systems, interleukin-(IL)-4 induces the secretion of IgG1 (ref. 1) and IgE (ref. 2); IL-5 enhances the secretion of IgA, and interferon-gamma (IFN-gamma) enhances the secretion of IgG2a (ref. 5). Clones of murine TH cells can be divided into two subsets, TH1 and TH2 (ref. 6). Both subsets synthesize IL-3 and granulocyte-monocyte colony-stimulating factor (GM-CSF), but only TH1 clones produce IL-2, IFN-gamma, and lymphotoxin (LT) and TH2 clones produce IL-4 and IL-5 (ref. 7). We have examined the role of clones of antigen-specific TH1 and TH2 cells in the regulation of the subclasses of IgG antibody secreted by antigen-specific B cells. Our results show that both types of TH cells induce the secretion of IgM and IgG3, whereas clones of TH1 and TH2 cells specifically induce antigen-specific B cells to secrete IgG2a and IgG1, respectively. We also demonstrate that regulation of commitment to the secretion of a particular IgG isotype occurs in two distinct stages: cognate interaction between T and B cells and interaction between T-cell-derived lymphokines and B cells.

MeSH terms

  • Animals
  • Antibody Formation*
  • B-Lymphocytes / immunology*
  • Epitopes
  • Immunoglobulin G / biosynthesis*
  • Immunoglobulin Isotypes / biosynthesis*
  • Interferon-gamma / pharmacology
  • Interleukin-2 / pharmacology
  • Interleukin-4
  • Interleukins / pharmacology
  • Lymphocyte Cooperation
  • Lymphokines / physiology
  • Mice
  • T-Lymphocytes, Helper-Inducer / immunology*
  • Trinitrobenzenes / immunology


  • Epitopes
  • Immunoglobulin G
  • Immunoglobulin Isotypes
  • Interleukin-2
  • Interleukins
  • Lymphokines
  • Trinitrobenzenes
  • Interleukin-4
  • Interferon-gamma