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System for Efficacy and Cytotoxicity Screening of Inhibitors Targeting Intracellular Mycobacterium tuberculosis
09:57

System for Efficacy and Cytotoxicity Screening of Inhibitors Targeting Intracellular Mycobacterium tuberculosis

Published on: April 5, 2017

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

J E Pearl1, I M Orme, A M Cooper

  • 1Mycobacterial Research Laboratories, Department of Microbiology, Colorado State University, Fort Collins, CO 80523, USA.

Tubercle and Lung Disease : the Official Journal of the International Union Against Tuberculosis and Lung Disease
|February 13, 2001
PubMed

Insights

Tuberculosis patients often show reduced immune responses due to CD4 T cell apoptosis. This study found that CD95L is not responsible for this decline in cellular immunity during tuberculosis infection.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Cell Biology

Background:

  • Tuberculosis (TB) is characterized by diminished cellular immune responses to Mycobacterium tuberculosis.
  • Apoptosis of CD4 T cells is implicated in this loss of immune response.
  • The role of CD95 (Fas receptor) and its ligand (CD95L) in this process remains unclear.

Purpose of the Study:

  • To investigate the role of CD95L in mediating the apoptosis of antigen-specific lymphocytes during Mycobacterium tuberculosis infection.

Main Methods:

  • Systemic infection of mice with a mutated CD95L molecule with virulent Mycobacterium tuberculosis.
  • Comparison of cellular immune responses between CD95L mutant mice and control mice.

Main Results:

  • Both control and CD95L mutant mice showed a decline in cellular responses to mycobacterial antigens.
  • A slight delay in the loss of response was observed in the CD95L mutant mice.
  • The persistence of cellular responses was limited even in mutant mice.

Conclusions:

  • The decline in antigen-specific cellular responses during tuberculosis infection in mice is not dependent on CD95L.
  • CD95L does not appear to be the primary mediator of lymphocyte apoptosis in this context.

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