Abstract
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. © 2009 Elsevier Ltd. All rights reserved.
| Original language | English |
|---|---|
| Pages (from-to) | 147-155 |
| Number of pages | 8 |
| Journal | Seminars in Immunology |
| Volume | 21 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Jun 2009 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Homeostasis
- Infection history
- Innate immunity
- Lung
- Secondary bacterial pneumonia
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