Journal
SEMINARS IN IMMUNOLOGY
Volume 21, Issue 3, Pages 147-155Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.smim.2009.01.005
Keywords
Lung; Innate immunity; Homeostasis; Secondary bacterial pneumonia; Infection history
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Funding
- Medical Research Council [G0400795]
- National Institute of Health [AI070232-10]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U01AI070232] Funding Source: NIH RePORTER
- MRC [G0400795] Funding Source: UKRI
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Innate immunity at mucosal surfaces requires additional restraint to prevent inflammation to innocuous antigens or commensal microorganisms. The threshold above which airway macrophages become activated is raised by site-specific factors including the receptors for transforming growth factor beta, interleukin 10 and CD200; the ligands for which are produced by, or expressed on, respiratory epithelium. We discuss such site-specific regulation and how this is continually altered by prior infections. Resetting of innate reactivity represents a strategy for limiting excessive inflammation, but in some may pre-dispose to secondary bacterial pneumonia. (C) 2009 Elsevier Ltd. All rights reserved.
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