Evasion of innate and adaptive immunity by Mycobacterium tuberculosis

Michael F. Goldberg, Neeraj K. Saini, Steven A. Porcelli

Research output: Chapter in Book/Report/Conference proceedingChapter

5 Scopus citations


Mycobacterium tuberculosis is an extremely successful pathogen that appears to have coevolved with humans as its specific host species for thousands of years (1). This persistent relationship has uniquely shaped the mycobacterial genome to encode mechanisms that enable the bacilli to resist attack and elimination by the human immune system. Although both innate and adaptive immunity clearly modify the course of M. tuberculosis infection, this organism can persist and cause disease even in fully immunocompetent hosts. In addition, the currently available vaccine for prevention of tuberculosis, the attenuated Mycobacterium bovis strain known as bacille Calmette-Guérin (BCG), has proven largely ineffective despite widespread use. This resistance to host immunity most likely reflects a highly evolved and multifactorial ability of pathogenic mycobacteria to prevent or evade effective host responses. A more complete understanding of how this occurs will likely be crucial to the design and production of better vaccines for prevention of tuberculosis. In this review we summarize current knowledge and recent advances in the study of immune evasion by M. tuberculosis.

Original languageEnglish (US)
Title of host publicationMolecular Genetics of Mycobacteria
Number of pages26
ISBN (Electronic)9781683671008
ISBN (Print)9781555818838
StatePublished - Oct 22 2015


  • Adaptive immunity
  • Autophagy
  • C-type lectin receptor signaling
  • Mmunological decoys
  • Mycobacterium tuberculosis
  • Nod-like receptors signaling
  • Nuclear oligomerization domain signaling
  • Phagosome maturation
  • Secreted proteins
  • Toll-like receptor signaling

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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