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T cells from Programmed Death-1 deficient mice respond poorly to Mycobacterium tuberculosis infection

Sultan Tousif1, Yogesh Singh, Durbaka Vijaya Raghava Prasad

  • 1Immunology Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India.

Plos One
|May 19, 2011
PubMed
Abstract

Insights

Programmed Death-1 (PD-1) receptor deficiency increases susceptibility to tuberculosis in mice. PD-1 actually promotes mycobacterial clearance by enhancing T cell responses and macrophage autophagy.

Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Programmed Death-1 (PD-1) is typically considered a negative regulator of T cell activation, inhibiting responses in infections.
  • Its ligands, PD-L1 and PD-L2, mediate this inhibitory function, contributing to disease resistance in various models.

Purpose of the Study:

  • To investigate the role of PD-1 in the context of Mycobacterium tuberculosis (M. tb) infection.
  • To determine if PD-1's known inhibitory function extends to M. tb pathogenesis.

Main Methods:

  • Mice deficient in PD-1 (PD-1(-/-)) and wild-type littermates were infected with M. tb H37Rv via aerosol.
  • T cell proliferation, regulatory T cell numbers, mesenchymal stem cell recruitment, and macrophage autophagy markers were assessed.

Main Results:

  • PD-1 deficient mice exhibited increased susceptibility to M. tb infection compared to wild-type controls.
  • M. tb antigen-specific T cell proliferation was significantly reduced in PD-1 deficient mice.
  • Increased regulatory T cells, mesenchymal stem cell recruitment, and decreased autophagy marker LC3-B were observed in PD-1 deficient mice.

Conclusions:

  • Contrary to expectations, PD-1 does not inhibit but rather promotes T cell responses crucial for controlling M. tb infection.
  • PD-1 plays a protective role in mice by facilitating mycobacterial clearance, potentially through enhancing T cell proliferation and macrophage function.

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