Evasion of innate and adaptive immunity by Mycobacterium tuberculosis

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

Research output: Contribution to journalArticle

36 Citations (Scopus)

Abstract

Through thousands of years of reciprocal coevolution, Mycobacterium tuberculosis has become one of humanity's most successful pathogens, acquiring the ability to establish latent or progressive infection and persist even in the presence of a fully functioning immune system. The ability of M. tuberculosis to avoid immune-mediated clearance is likely to reflect a highly evolved and coordinated program of immune evasion strategies that interfere with both innate and adaptive immunity. These include the manipulation of their phagosomal environment within host macrophages, the selective avoidance or engagement of pattern recognition receptors, modulation of host cytokine production, and themanipulation of antigen presentation to prevent or alter the quality of T-cell responses. In this article we review an extensive array of published studies that have begun to unravel the sophisticated program of specific mechanisms that enable M. tuberculosis and other pathogenic mycobacteria to persist and replicate in the face of considerable immunological pressure from their hosts. Unraveling the mechanisms by which M. tuberculosis evades or modulates host immune function is likely to be of major importance for the development of more effective new vaccines and targeted immunotherapy against tuberculosis.

Original languageEnglish (US)
Article numberMGM2-0005-2013
JournalMicrobiology spectrum
Volume2
Issue number5
DOIs
StatePublished - 2014

Fingerprint

tuberculosis
Adaptive Immunity
immunity
Mycobacterium tuberculosis
Innate Immunity
Immune Evasion
Pattern Recognition Receptors
Antigen Presentation
Mycobacterium
Immunotherapy
pattern recognition
vaccine
coevolution
immune system
Immune System
antigen
Tuberculosis
Vaccines
Macrophages
Cytokines

ASJC Scopus subject areas

  • Immunology and Microbiology(all)
  • Infectious Diseases
  • Microbiology (medical)
  • Ecology
  • Cell Biology
  • Genetics
  • Physiology

Cite this

Evasion of innate and adaptive immunity by Mycobacterium tuberculosis. / Goldberg, Michael F.; Saini, Neeraj K.; Porcelli, Steven A.

In: Microbiology spectrum, Vol. 2, No. 5, MGM2-0005-2013, 2014.

Research output: Contribution to journalArticle

@article{a2c15a4f00d34518a019e864bc40cf3e,
title = "Evasion of innate and adaptive immunity by Mycobacterium tuberculosis",
abstract = "Through thousands of years of reciprocal coevolution, Mycobacterium tuberculosis has become one of humanity's most successful pathogens, acquiring the ability to establish latent or progressive infection and persist even in the presence of a fully functioning immune system. The ability of M. tuberculosis to avoid immune-mediated clearance is likely to reflect a highly evolved and coordinated program of immune evasion strategies that interfere with both innate and adaptive immunity. These include the manipulation of their phagosomal environment within host macrophages, the selective avoidance or engagement of pattern recognition receptors, modulation of host cytokine production, and themanipulation of antigen presentation to prevent or alter the quality of T-cell responses. In this article we review an extensive array of published studies that have begun to unravel the sophisticated program of specific mechanisms that enable M. tuberculosis and other pathogenic mycobacteria to persist and replicate in the face of considerable immunological pressure from their hosts. Unraveling the mechanisms by which M. tuberculosis evades or modulates host immune function is likely to be of major importance for the development of more effective new vaccines and targeted immunotherapy against tuberculosis.",
author = "Goldberg, {Michael F.} and Saini, {Neeraj K.} and Porcelli, {Steven A.}",
year = "2014",
doi = "10.1128/microbiolspec.MGM2-0005-2013",
language = "English (US)",
volume = "2",
journal = "Microbiology spectrum",
issn = "2165-0497",
publisher = "American Society for Microbiology",
number = "5",

}

TY - JOUR

T1 - Evasion of innate and adaptive immunity by Mycobacterium tuberculosis

AU - Goldberg, Michael F.

AU - Saini, Neeraj K.

AU - Porcelli, Steven A.

PY - 2014

Y1 - 2014

N2 - Through thousands of years of reciprocal coevolution, Mycobacterium tuberculosis has become one of humanity's most successful pathogens, acquiring the ability to establish latent or progressive infection and persist even in the presence of a fully functioning immune system. The ability of M. tuberculosis to avoid immune-mediated clearance is likely to reflect a highly evolved and coordinated program of immune evasion strategies that interfere with both innate and adaptive immunity. These include the manipulation of their phagosomal environment within host macrophages, the selective avoidance or engagement of pattern recognition receptors, modulation of host cytokine production, and themanipulation of antigen presentation to prevent or alter the quality of T-cell responses. In this article we review an extensive array of published studies that have begun to unravel the sophisticated program of specific mechanisms that enable M. tuberculosis and other pathogenic mycobacteria to persist and replicate in the face of considerable immunological pressure from their hosts. Unraveling the mechanisms by which M. tuberculosis evades or modulates host immune function is likely to be of major importance for the development of more effective new vaccines and targeted immunotherapy against tuberculosis.

AB - Through thousands of years of reciprocal coevolution, Mycobacterium tuberculosis has become one of humanity's most successful pathogens, acquiring the ability to establish latent or progressive infection and persist even in the presence of a fully functioning immune system. The ability of M. tuberculosis to avoid immune-mediated clearance is likely to reflect a highly evolved and coordinated program of immune evasion strategies that interfere with both innate and adaptive immunity. These include the manipulation of their phagosomal environment within host macrophages, the selective avoidance or engagement of pattern recognition receptors, modulation of host cytokine production, and themanipulation of antigen presentation to prevent or alter the quality of T-cell responses. In this article we review an extensive array of published studies that have begun to unravel the sophisticated program of specific mechanisms that enable M. tuberculosis and other pathogenic mycobacteria to persist and replicate in the face of considerable immunological pressure from their hosts. Unraveling the mechanisms by which M. tuberculosis evades or modulates host immune function is likely to be of major importance for the development of more effective new vaccines and targeted immunotherapy against tuberculosis.

UR - http://www.scopus.com/inward/record.url?scp=84958824786&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84958824786&partnerID=8YFLogxK

U2 - 10.1128/microbiolspec.MGM2-0005-2013

DO - 10.1128/microbiolspec.MGM2-0005-2013

M3 - Article

C2 - 26104343

AN - SCOPUS:84958824786

VL - 2

JO - Microbiology spectrum

JF - Microbiology spectrum

SN - 2165-0497

IS - 5

M1 - MGM2-0005-2013

ER -