Tumor necrosis factor (TNF) receptor type 2 mediates thymocyte proliferation independently of TNF receptor type 1

Eur J Immunol. 1998 Jan;28(1):257-63. doi: 10.1002/(SICI)1521-4141(199801)28:01<257::AID-IMMU257>3.0.CO;2-G.

Abstract

Tumor necrosis factor (TNF) mediates its biological effects by binding to two distinct but homologous receptor molecules. The type 1 receptor (TNF-R1) has been shown to be essential and sufficient for most cellular responses to soluble TNF. In contrast, only limited data exist concerning the role of the type 2 receptor (TNF-R2) in TNF responses, both in vitro and in vivo. Here, we demonstrate by the use of thymocytes from TNF-R-deficient mice that the TNF-R2-dependent enhancement of proliferation and secretion of granulocyte-macrophage colony-stimulating factor is in fact mediated by TNF-R2 on its own, independent of co-expression and/or stimulation of TNF-R1.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigens, CD / genetics
  • Antigens, CD / metabolism
  • Antigens, CD / physiology*
  • Concanavalin A / pharmacology
  • Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
  • Humans
  • Lymphocyte Activation*
  • Mice
  • Mice, Knockout
  • Receptors, Tumor Necrosis Factor / genetics
  • Receptors, Tumor Necrosis Factor / metabolism
  • Receptors, Tumor Necrosis Factor / physiology*
  • Receptors, Tumor Necrosis Factor, Type I
  • Receptors, Tumor Necrosis Factor, Type II
  • Recombinant Proteins / pharmacology
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • Thymus Gland / cytology
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Antigens, CD
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Type I
  • Receptors, Tumor Necrosis Factor, Type II
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Concanavalin A
  • Granulocyte-Macrophage Colony-Stimulating Factor