IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 18264110.
- Also identified by DOI 10.1038/nm1710 and PMC identifier 2901867.
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Abstract
Emerging evidence supports the concept that T helper type 17 (T(H)17) cells, in addition to mediating autoimmunity, have key roles in mucosal immunity against extracellular pathogens. Interleukin-22 (IL-22) and IL-17A are both effector cytokines produced by the T(H)17 lineage, and both were crucial for maintaining local control of the Gram-negative pulmonary pathogen, Klebsiella pneumoniae. Although both cytokines regulated CXC chemokines and granulocyte colony-stimulating factor production in the lung, only IL-22 increased lung epithelial cell proliferation and increased transepithelial resistance to injury. These data support the concept that the T(H)17 cell lineage and its effector molecules have evolved to effect host defense against extracellular pathogens at mucosal sites.
Medical subject headings
- Immunity, Mucosal
- Interleukins
- Klebsiella Infections
- Klebsiella pneumoniae