CD95 signaling is not required for the down regulation of cellular responses to systemic Mycobacterium tuberculosis infection

Tuber Lung Dis. 2000;80(6):273-9. doi: 10.1054/tuld.2000.0274.

Abstract

There is a tendency among tuberculosis patients to have reduced cellular responses to mycobacterial antigens and this loss has been associated with apoptosis of CD4 T cells. In order to determine the role of CD95 in mediating apoptosis of antigen-specific lymphocytes in tuberculosis, mice with a mutated CD95L molecule were infected systemically with virulent Mycobacterium tuberculosis. Both control and CD95L mutant mice exhibited the expected loss of response to mycobacterial antigens, with the only difference being a slight delay in the loss of the response in the mutant mice. The limited persistence of the response in the mutant mice suggests that, while antigen-specific cellular responses do decline in mice infected with mycobacteria, this decline is not dependent upon CD95L.

Publication types

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

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Colony Count, Microbial
  • Colorimetry
  • Down-Regulation / physiology*
  • Enzyme-Linked Immunosorbent Assay
  • Fas Ligand Protein
  • Flow Cytometry
  • Immunity, Cellular / physiology
  • Lymphocyte Activation
  • Membrane Glycoproteins / genetics*
  • Mice
  • Mice, Inbred C57BL
  • Mutation
  • Mycobacterium tuberculosis / isolation & purification
  • T-Lymphocyte Subsets / immunology*
  • Tuberculosis / immunology*
  • fas Receptor / immunology*

Substances

  • Fas Ligand Protein
  • Fasl protein, mouse
  • Membrane Glycoproteins
  • fas Receptor