A tailless fas-FADD death-effector domain chimera is sufficient to execute Fas function in T cells but not B cells of MRL-lpr/lpr mice

J Immunol. 1999 Mar 1;162(5):2766-74.

Abstract

The Fas receptor delivers signals crucial for lymphocyte apoptosis through its cytoplasmic death domain. Several Fas cytoplasmic-associated proteins have been reported and studied in cell lines. So far, only Fas-associated death domain protein (FADD), another death domain-containing molecule has been shown to be essential for Fas signals in vivo. FADD is thought to function by recruiting caspase-8 through its death-effector domain. To test whether FADD is sufficient to deliver Fas signals, we generated transgenic mice expressing a chimera comprised of the Fas extracellular domain and FADD death-effector domain. Expression of this protein in lymphocytes of Fas-deficient MRL-lpr/lpr mice completely diminishes their T cell but not their B cell abnormalities. These results suggest that FADD alone is sufficient for initiation of Fas signaling in primary T cells, but other pathways may operate in B cells.

Publication types

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

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Animals
  • B-Lymphocytes / physiology*
  • Carrier Proteins / physiology*
  • Fas-Associated Death Domain Protein
  • Humans
  • Immunoglobulin G / blood
  • Immunoglobulin G / classification
  • Jurkat Cells
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred MRL lpr
  • Mice, Transgenic
  • Recombinant Fusion Proteins / physiology*
  • Splenomegaly / etiology
  • T-Lymphocytes / physiology*
  • fas Receptor / physiology*

Substances

  • Adaptor Proteins, Signal Transducing
  • Carrier Proteins
  • FADD protein, human
  • Fadd protein, mouse
  • Fas-Associated Death Domain Protein
  • Immunoglobulin G
  • Recombinant Fusion Proteins
  • fas Receptor