Interleukin-12 regulates the proliferation of Th1, but not Th2 or Th0, clones

Eur J Immunol. 1994 Oct;24(10):2271-8. doi: 10.1002/eji.1830241002.

Abstract

Our results indicate that interleukin (IL)-12 is an important costimulator of antigen-dependent proliferation of murine Th1 clones. In addition, we demonstrate that IL-10 inhibits splenic antigen-presenting cell (APC)-dependent proliferation of Th1 clones, at least in part, via down-regulation of APC-derived IL-12. Moreover, the failure of activated B cells to provide costimulation via IL-12 accounts for their inability to support optimal proliferative responses of Th1 clones. We also show that IL-12 regulates the ability of Th1 clones to respond to IL-4 and enhances their proliferation in response to IL-2, IL-7, or IL-15. In contrast, Th2 and Th0 clones appear refractory to the effects of IL-12, on antigen-dependent or growth factor-induced proliferation.

MeSH terms

  • Animals
  • Antigen-Presenting Cells / immunology
  • Antigens / immunology
  • B-Lymphocytes / immunology
  • Clone Cells
  • Female
  • Interleukin-10 / pharmacology
  • Interleukin-12 / pharmacology*
  • Interleukin-2 / biosynthesis
  • Interleukin-4 / pharmacology
  • Lymphocyte Activation / drug effects*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred Strains
  • T-Lymphocyte Subsets / immunology*
  • T-Lymphocytes, Helper-Inducer / immunology*

Substances

  • Antigens
  • Interleukin-2
  • Interleukin-10
  • Interleukin-12
  • Interleukin-4