| Literature DB >> 18714018 |
Satoru Hamada1, Masayuki Umemura, Takeru Shiono, Kensho Tanaka, Ayano Yahagi, M Dilara Begum, Kiyotetsu Oshiro, Yuko Okamoto, Hisami Watanabe, Kazuyoshi Kawakami, Christina Roark, Willi K Born, Rebecca O'Brien, Koichi Ikuta, Hiromichi Ishikawa, Susumu Nakae, Yoichiro Iwakura, Takao Ohta, Goro Matsuzaki.
Abstract
IL-17A is originally identified as a proinflammatory cytokine that induces neutrophils. Although IL-17A production by CD4(+) Th17 T cells is well documented, it is not clear whether IL-17A is produced and participates in the innate immune response against infections. In the present report, we demonstrate that IL-17A is expressed in the liver of mice infected with Listeria monocytogenes from an early stage of infection. IL-17A is important in protective immunity at an early stage of listerial infection in the liver because IL-17A-deficient mice showed aggravation of the protective response. The major IL-17A-producing cells at the early stage were TCR gammadelta T cells expressing TCR Vgamma4 or Vgamma6. Interestingly, TCR gammadelta T cells expressing both IFN-gamma and IL-17A were hardly detected, indicating that the IL-17A-producing TCR gammadelta T cells are distinct from IFN-gamma-producing gammadelta T cells, similar to the distinction between Th17 and Th1 in CD4(+) T cells. All the results suggest that IL-17A is a newly discovered effector molecule produced by TCR gammadelta T cells, which is important in innate immunity in the liver.Entities:
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Year: 2008 PMID: 18714018 PMCID: PMC2859669 DOI: 10.4049/jimmunol.181.5.3456
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422