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NKT cells as an interface between bacterial infection and neutrophil-mediated host protective response

学友会セミナー

学友会セミナー

2004年開催 学友会セミナー

開催日時: 平成16年11月1日(月)  10:00 ~ 10:45
開催場所: アムジェンホール 大会議室
講  師: 川 上 和 義 先生
所  属: 琉球大学大学院医学研究科感染病態制御学講座 分子病態感染症学文分野(第一内科)
演  題: NKT cells as an interface between bacterial infection and neutrophil-mediated host protective response
概  要:

Recently, many investigators have explored the role of NKT cells in the host defense to various infectious pathogens. We previously reported the different role of Valpha14+ NKT cells in the protective response against Cryptococcus neoformans and Mycobacterium tuberculosis, both of which are intracellular microorganisms.

We have extended these studies to understand the role of NKT cells in the host defense to extracellular bacteria such as Streptococcus pneumoniae, in which neutrophils play a major contribution as the killing effector cells.

For this purpose, we examined the effect of lack in Valpha14+ NKT cells on the clinical course of pulmonary infection with this bacterium using Jalpha281KO mice. These mice were highly susceptible to S. pneumoniae infection, which was well correlated with the impaired neutrophil-mediated inflammatory responses. IFN-gamma synthesis was detected at a considerable level in lungs as quickly as at 1 hr post-infection. These observations suggest a possible involvement of this cytokine in the protective role of NKT cells. Compatibly, administration of rIFN-gamma resulted in the recovery of impaired host defense in Jalpha281KO mice. Furthermore, transfer of liver mononuclear cells (LMNC) from wild type mice canceled this impairment, while such phenomenon was not observed in the transfer with LMNC from either Jalpha281KO or GKO mice.

Our study clearly demonstrate the critical role of Valpha14 subset of NKT cells in the neutrophil-mediated host defense to some extacellular bacteria and raise a possibility that these cells may contribute to the protective response through inducing the production of IFN-gamma.

世 話 人: 免疫調節分野 高津 聖志
感染遺伝学分野 三宅 健介