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The role of IL-10 in immune regulation during M. tuberculosis infection

Journal

MUCOSAL IMMUNOLOGY
Volume 4, Issue 3, Pages 261-270

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2011.7

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Funding

  1. Medical Research Council, UK
  2. NIH [AI62921, P30 CA21765]
  3. Hartwell Foundation
  4. American Lebanese Syrian Associated Charities
  5. MRC [MC_U117565642] Funding Source: UKRI
  6. Medical Research Council [MC_U117565642] Funding Source: researchfish

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During gaseous exchange the lungs are exposed to a vast variety of pathogens, allergens, and innocuous particles. A feature of the lung immune response to lung-tropic aerosol-transmitted bacteria such as Mycobacterium tuberculosis (Mtb) is a balanced immune response that serves to restrict pathogen growth while not leading to host-mediated collateral damage of the delicate lung tissues. One immune-limiting mechanism is the inhibitory and anti-inflammatory cytokine interleukin (IL)-10. IL-10 is made by many hematopoietic cells and a major role is to suppress macrophage and dendritic cell (DC) functions, which are required for the capture, control, and initiation of immune responses to pathogens such as Mtb. Here, we review the role of IL-10 on bacterial control during the course of Mtb infection, from early innate to adaptive immune responses. We propose that IL-10 is linked with the ability of Mtb to evade immune responses and mediate long-term infections in the lung.

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