Publication: Regulation of Neutrophils by Interferon-\(\gamma\) Limits Lung Inflammation During Tuberculosis Infection
Open/View Files
Date
2011
Authors
Published Version
Journal Title
Journal ISSN
Volume Title
Publisher
The Rockefeller University Press
The Harvard community has made this article openly available. Please share how this access benefits you.
Citation
Nandi, Bisweswar, and Samuel M. Behar. 2011. Regulation of neutrophils by interferon-\(\gamma\) limits lung inflammation during tuberculosis infection. The Journal of Experimental Medicine 208(11): 2251-2262.
Research Data
Abstract
Resistance to Mycobacterium tuberculosis requires the host to restrict bacterial replication while preventing an over-exuberant inflammatory response. Interferon (IFN) \(\gamma\) is crucial for activating macrophages and also regulates tissue inflammation. We dissociate these two functions and show that IFN-\(\gamma^{−/−}\) memory CD4\(^+\) T cells retain their antimicrobial activity but are unable to suppress inflammation. IFN-\(\gamma\) inhibits CD4\(^+\) T cell production of IL-17, which regulates neutrophil recruitment. In addition, IFN-\(\gamma\) directly inhibits pathogenic neutrophil accumulation in the infected lung and impairs neutrophil survival. Regulation of neutrophils is important because their accumulation is detrimental to the host. We suggest that neutrophilia during tuberculosis indicates failed Th1 immunity or loss of IFN-\(\gamma\) responsiveness. These results establish an important antiinflammatory role for IFN-\(\gamma\) in host protection against tuberculosis.
Description
Other Available Sources
Keywords
CD8(+) T-cells, experimental autoimmune encephalomyelitis, Calmette-Guérin infection, mycobacterium-tuberculosis, IFN-\(\gamma\), immune responses, in-vivo, mice, receptor, expression
Terms of Use
This article is made available under the terms and conditions applicable to Other Posted Material (LAA), as set forth at Terms of Service