Author: ["Shean J Aujla","Yvonne R Chan","Mingquan Zheng","Mingjian Fei","David J Askew","Derek A Pociask","Todd A Reinhart","Florencia McAllister","Jennifer Edeal","Kristi Gaus","Shahid Husain","James L Kreindler","Patricia J Dubin","Joseph M Pilewski","Mike M Myerburg","Carol A Mason","Yoichiro Iwakura","Jay K Kolls"]
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Abstract
Emerging evidence supports the concept that T helper type 17 (TH17) 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 TH17 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 TH17 cell lineage and its effector molecules have evolved to effect host defense against extracellular pathogens at mucosal sites.Cite this article
Aujla, S., Chan, Y., Zheng, M. et al. IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia. Nat Med 14, 275–281 (2008). https://doi.org/10.1038/nm1710 