Keio University · 생화학·유전·분자생물학
켄야 온다 교수의 연구실은 장내 미생물과 숙주 면역 시스템 간의 상호작용을 중심으로, 특히 구강 출처의 박테리아가 장에서 비정상적으로 정착할 경우 유도하는 면역 반응과 만성 염증성 질환의 기전을 규명하는 데 주력하고 있습니다. TLR 및 type I 인터페론 경로를 중심으로 면역세포의 활성화 메커니즘과, 바이러스 감염에 대한 면역 반응 조절 원리에 대한 기초 생물학적 연구도 진행 중입니다. 이는 장내 미생물군집의 변화가 면역질환과 어떻게 연관되는지를 밝혀내는 데 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Intestinal colonization by bacteria of oral origin has been correlated with several negative health outcomes, including inflammatory bowel disease. However, a causal role of oral bacteria ectopically colonizing the intestine remains unclear. Using gnotobiotic techniques, we show that strains of <i>Klebsiella</i> spp. isolated from the salivary microbiota are strong inducers of T helper 1 (T<sub>H</sub>1) cells when they colonize in the gut. These <i>Klebsiella</i> strains are resistant to multip
The mammalian alimentary tract harbors hundreds of species of commensal microorganisms (microbiota) that intimately interact with the host and provide it with genetic, metabolic, and immunological attributes. Recent reports have indicated that the microbiota composition and its collective genomes (microbiome) are major factors in predetermining the type and robustness of mucosal immune responses. In this review, we discuss the recent advances in our understanding of host-microbiota interactions
Toll-like receptor (TLR) activation is central to immunity, wherein the activation of the TLR9 subfamily members TLR9 and TLR7 results in the robust induction of type I IFNs (IFN-alpha/beta) by means of the MyD88 adaptor protein. However, it remains unknown how the TLR signal "input" can be processed through MyD88 to "output" the induction of the IFN genes. Here, we demonstrate that the transcription factor IRF-7 interacts with MyD88 to form a complex in the cytoplasm. We provide evidence that t
A complex mechanism may be operational for dendritic cell (DC) maturation, wherein Toll-like receptor and other signaling pathways may be coordinated differently depending on the nature of the pathogens, in order for DC maturation to be most effective to a given threat. Here, we show that IFN-alpha/beta signaling is selectively required for the maturation of DCs induced by double-stranded RNA or viral infection in vitro. Interestingly, the maturation is still observed in the absence of either of
The type I IFN-alpha/beta gene family was identified about a quarter of a century ago as a prototype of many cytokine gene families, which led to the subsequent burst of studies on molecular mechanisms underlying cytokine gene expression and signaling. Although originally discovered for their activity to confer an antiviral state on cells, more evidence has recently been emerging regarding IFN-alpha/beta actions on cell growth, differentiation and many immunoregulatory activities, which are of e
