IL-22はグラム陰性菌による肺炎に対する粘膜感染防御を仲介する

（nature medicine 3月号Vol.14 No.2 / P.275 - 281）

IL-22はグラム陰性菌による肺炎に対する粘膜感染防御を仲介する

17型ヘルパーT （TH17）細胞は、自己免疫に関与するだけでなく、
細胞外増殖性の病原体に対する粘膜免疫でも中心的な役割を
担っているという考えを支持。

インターロイキン22（IL-22）とIL-17Aは、TH17細胞によって産生される
エフェクターサイトカインで、グラム陰性の肺炎桿菌である
Klebsiella pneumoniaeの局所における感染制御に両方共に重要。

これらのサイトカインは、肺におけるCXCケモカインと
顆粒球コロニー刺激因子の産生を促進したが、
IL-22のみが肺上皮細胞増殖と損傷に対する上皮細胞の修復能力を高めた。

これらのデータは、TH17細胞とそのエフェクター分子が
細胞外病原体に対する粘膜における感染防御にあたるために
進化してきたという考えを支持する。

[原文]
IL-22 mediates mucosal host defense against Gram-negative bacterial pneumonia

Shean J Aujla1, Yvonne R Chan2, Mingquan Zheng1, Mingjian Fei1, David J Askew3, Derek A Pociask1, Todd A Reinhart4, Florencia McAllister1, Jennifer Edeal1, Kristi Gaus4, Shahid Husain5, James L Kreindler1, Patricia J Dubin1, Joseph M Pilewski2, Mike M Myerburg2, Carol A Mason6, Yoichiro Iwakura7& Jay K Kolls1

1Children's Hospital of Pittsburgh, Suite 3765, 3705 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
2Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, 3459 Fifth Avenue, 628 Northwest, Pittsburgh, Pennsylvania 15213, USA.
3University of Pittsburgh Medical Center Newborn Medicine Program, Children's Hospital of Pittsburgh and Magee-Women's Research Institute, 300 Halket Street, Pittsburgh, Pennsylvania 15213, USA.
4Department of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh, 130 DeSoto Street, Pittsburgh, Pennsylvania 15261, USA.
5　Division of Infectious Diseases, Transplant Infectious Disease Unit, University of Pittsburgh Medical Center, 3601 Fifth Avenue, Pittsburgh, Pennsylvania 15213, USA.
6　Division of Pulmonary and Critical Care Medicine, Louisiana Health Sciences Center, New Orleans, 1901 Perdido Street, Louisiana 70112, USA.
7　Center for Experimental Medicine, The Institute of Medical Science, The University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan

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.

http://www.m3.com/tools/MedicalLibrary/nature/200803/nature_medicine/04.html