大阪大学 · Medicine
아츠시 쿠마노고 교수의 연구실은 면역계의 세포 간 신호전달 메커니즘, 특히 CD40-CD40L 및 CD100와 같은 세밀한 면역조절 분자들이 자가면역질환과 세균성 면역 반응에 미치는 영향을 중심으로 연구를 진행하고 있습니다. 주로 항체 반응과 T세포 반응의 조절 메커니즘을 밝혀내며, 이는 자가면역질환의 발병 기전 규명과 새로운 치료 전략 개발에 기여하고자 합니다. 특히 면역세포의 활성화 및 항원 처리 과정에서 핵심적인 역할을 하는 분자들에 대한 기초 생물학적 연구를 꾸준히 수행하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
This work was supported by Japan Society for the Promotion of Science KAKENHI (JP17K16045, JP18H05282, and JP15K09220), Japan Agency for Medical Research and Development (JP17cm0106310, JP18cm0106335 and JP18cm059042), and Core Research for Evolutional Science and Technology (JPMJCR16G2).
Mutations in the CD40 ligand (CD40L) gene lead to X-linked immunodeficiency with hyper-IgM, which is often associated with autoimmune diseases. To determine the contribution of defective CD40-CD40L interactions to T cell autoreactivity, we reconstituted CD40-CD40L interactions by transferring T cells from CD40-deficient mice to syngenic athymic nude mice and assessed autoimmunity. T cells from CD40-deficient mice triggered autoimmune diseases accompanied with elevations of various autoantibodies
Abstract CD100 belongs to the semaphorin family, several members of which are known to act as repulsive axonal guidance factors during neuronal development. We have previously demonstrated that CD100 plays a crucial role in humoral immunity. In this study, we show that CD100 is also important for cellular immunity through the maturation of dendritic cells (DCs). CD100−/− mice fail to develop experimental autoimmune encephalomyelitis induced by myelin oligodendrocyte glycoprotein peptide, because
