Nagoya University · 의학
Keiko Kataoka 교수의 연구실은 장내 미생물군과 숙주의 면역 반응 간의 상호작용이 만성 염증성 질환 및 신경퇴행성 질환에 미치는 영향을 중심으로 연구를 진행하고 있습니다. 특히 망막 질환에서 면역세포의 활성화, 인플라마좀의 역할, 그리고 혈관 형성과 관련된 면역 조절 메커니즘을 밝혀내는 데 초점을 맞추고 있습니다. 이는 장-장기 축의 면역 조절 메커니즘을 이해하고, 새로운 치료 전략 개발에 기여하고자 하는 목적이 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
The role of the intestinal microbiota in human health is gaining more attention since clear changes in the composition of the intestinal bacteria or environment are seen in patients with inflammatory bowel disease, allergy, autoimmune disease, and some lifestyle-related illnesses. A healthy gut environment is regulated by the exquisite balance of intestinal microbiota, metabolites, and the host's immune system. Imbalance of these factors in genetically susceptible persons may promote a disease s
Although (1-->3)-beta-d-glucans, which are one of major fungal cell wall components, are known to activate invertebrate innate immune systems, their activities on mammalian cells remain elusive. Here, we report their activities on mouse macrophages. Among the various (1-->3)-beta-d-glucans, curdlan, a linear (1-->3)-beta-d-glucan, although not branched beta-glucans, exhibits significant activity to stimulate nuclear factor-kappaB in macrophages. The activity of curdlan is dramatically enhanced b
Vitreal macrophages are attracted to the site of pathologic angiogenesis triggered by retinal ischemia, where they actively participate in vascular development.
Detachment of photoreceptors from the retinal pigment epithelium is seen in various retinal disorders, resulting in photoreceptor death and subsequent vision loss. Cell death results in the release of endogenous molecules that activate molecular platforms containing caspase-1, termed inflammasomes. Inflammasome activation in retinal diseases has been reported in some cases to be protective and in others to be detrimental, causing neuronal cell death. Moreover, the cellular source of inflammasome
OCTA revealed that the vessel junction densities of type 1 CNVs were lower than those of type 2 CNVs, suggesting type 1 CNV vessels are more mature than type 2 CNV vessels.