SRC 연구자 여러분 안녕하세요,

다가오는 새 해 2020년 1월 SRC 세미나 안내입니다.

2020년 첫 세미나는 1월 10일 금요일 오후 6시 Weill Cornell Belfer 1401 호에서 진행될 예정이며, 

이번 세미나는 NYU의 Dan R. Littman 실험실에 계신 이준용 박사님께서 “Serum Amyloid A Proteins Induce Pathogenic TH17 Cells and Promote Inflammatory Disease”의 주제로 발표를 해주시기로 했습니다.

아시는 분들도 계시겠지만, Dan R. Littman 실험실(https://www.littmanlab.org/)은 장내 환경 (Microbiota, metabolite)이 어떻게 인체 면역을 조절하는지에 대한 연구를 진행하고 있는 연구실로, 특히 Th17세포 연구분야를 이끌고 있는 실험실입니다. 2017년 여성의 장내미생물이 자폐증 아이의 출산에 직접적인 영향을 미친다는 사실을 규명해서 더 잘 알려진 하버드대 허준열 교수님도 본 연구실 출신이십니다.

특히, 본 발표는 이번 12월 19일 Cell에 게재된 최신 연구결과에 대한 발표로, Th17 세포의 분화/활성을 조절하는 인체 내 면역조절 시스템에 대한 깊이 있는 지식을 얻을 수 있는 아주 유익한 시간이 될 것이라 사료됩니다. 자세한 내용은 아래 초록 또는 아래 링크를 확인하실 수 있습니다.

https://www.sciencedirect.com/science/article/pii/S0092867419312838?fbclid=IwAR23mrFCBsLlCfjkkWKYVvPS6EfK8K4BQozRjJuNhbQNqBPXg9ZidiDT34s

아무조록 새해를 시작하는 첫 세미나인 만큼 많은 분들께서 참여해주셔서,

유익한 세미나도 듣고, 좋은 네트워킹도 형성 할 수 있는 시간이 되길 바랍니다.

충분한 음식 준비를 위해 아래 링크에RSVP를 꼭 부탁드립니다.  

https://doodle.com/poll/zii5aiqkigaib4bp

그럼 2019년 한해 마무리 잘하시고,

다가오는 새해에도 하시는 모든일이 잘 되시길 기원하겠습니다.

1월 세미나에서 직접 만나뵙도록 하겠습니다. 

SRC 회장단 백정은, 박민주, 강설희 드림. 

Title : Serum Amyloid A Proteins Induce Pathogenic TH17 Cells and Promote Inflammatory Disease

Summary: Lymphoid cells that produce IL-17 cytokines protect barrier tissues from pathogenic microbes, but are also prominent effectors of inflammation and autoimmune disease. T-helper (TH17) cells, defined by RORgt-dependent production of IL-17A and IL-17F, exert homeostatic functions in the gut upon microbiota-directed differentiation from naïve CD4+ T cells. In the non-pathogenic setting, their cytokine production is regulated by serum amyloid A proteins (SAA1 and SAA2) secreted by adjacent intestinal epithelial cells. However, TH17 cell behaviors vary markedly according to their environment. Here we show that SAAs additionally direct a pathogenic pro-inflammatory TH17 cell differentiation program, acting directly on T cells in collaboration with STAT3-activating cytokines. Using loss- and gain-of-function mouse models, we show that SAA1, SAA2, and SAA3 have distinct systemic and local functions in promoting TH17-mediated inflammatory diseases. These studies suggest that T cell signaling pathways modulated by the SAAs may be attractive targets for anti-inflammatory therapies.