期刊
NATURE MEDICINE
卷 14, 期 3, 页码 275-281出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm1710
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资金
- NCATS NIH HHS [UL1 TR000005] Funding Source: Medline
- NHLBI NIH HHS [5R01HL079142, R01 HL061271, R01 HL079142, P50 HL084932, R01 HL061271-04, R37 HL079142, P50HL084932, R01 HL079142-04] Funding Source: Medline
- NIDDK NIH HHS [P30 DK072506, P30DK072506] Funding Source: Medline
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.
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