Cell-mediated Immune Responses in Tuberculosis

Annu Rev Immunol. 2009;27:393-422. doi: 10.1146/annurev.immunol.021908.132703.

Abstract

Tuberculosis is primarily a disease of the lung, and dissemination of the disease depends on productive infection of this critical organ. Upon aerosol infection with Mycobacterium tuberculosis (Mtb), the acquired cellular immune response is slow to be induced and to be expressed within the lung. This slowness allows infection to become well established; thus, the acquired response is expressed in an inflammatory site that has been initiated and modulated by the bacterium. Mtb has a variety of surface molecules that interact with the innate response, and this interaction along with the autoregulation of the immune response by several mechanisms results in less-than-optimal control of bacterial growth. To improve current vaccine strategies, we must understand the factors that mediate induction, expression, and regulation of the immune response in the lung. We must also determine how to induce both known and novel immunoprotective responses without inducing immunopathologic consequences.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • B-Lymphocytes / immunology*
  • B-Lymphocytes / metabolism
  • B-Lymphocytes / microbiology
  • Cytokines / immunology
  • Cytokines / metabolism
  • Humans
  • Immunity, Cellular / immunology*
  • Immunologic Memory
  • Macrophages / immunology*
  • Macrophages / metabolism
  • Macrophages / microbiology
  • Mycobacterium tuberculosis / pathogenicity*
  • Receptors, Pattern Recognition / immunology
  • Receptors, Pattern Recognition / metabolism
  • T-Lymphocyte Subsets / immunology*
  • T-Lymphocyte Subsets / metabolism
  • T-Lymphocyte Subsets / microbiology
  • Tuberculosis / immunology*
  • Tuberculosis / metabolism
  • Tuberculosis / microbiology

Substances

  • Cytokines
  • Receptors, Pattern Recognition