SLAM is a microbial sensor that regulates bacterial phagosome function in macrophages (Nat Immunol, 2010, 11:920-927)

報告日期: 2010/11/02
報告時間: 16:00/16:50
報告學生: 蔡宗婷
講評老師: 林以行

Full text:

SLAM is a microbial sensor that regulates bacterial phagosome functions in macrophages


Berger, SB. et al. Nat Immunol. 11:920-7 (2010).


Speaker: 蔡宗婷

Commentator: 林以行老師

Time:2010/11/2 16:00-16:50

Place:Room 602




    Macrophages play the critical role in the host defense against microbial infection. Several receptors on macrophages can synchronize to recognize bacteria via conserved structures on the bacterial surface and then facilitate phagocytosis to initiates the innate immune response as well as triggers subsequent activation of adaptive immunity. However, how the cell surface receptors control key steps in microbicidal functions, such as the production of reactive oxygen species or phagolysosomal fusion is still unknown. SLAM is well known for its homotypic costimulatory molecule functions. In this study, the authors demonstrated SLAM, in addition to being a costimulatory molecule can act as a key regulator in the innate immune defense against Gram-negative bacteria in macrophages by participating in two microbicidal phagosomal processes: phagosome maturation and the production of free radical species by the NOX2 complex. SLAM first recognizes the outer membrane of most Gram-negative bacteria. Once SLAM binds the bacteria, it is actively dragged into the developing phagosome, where it is responsible for recruiting a complex containing Vps34, Vps15 and beclin-1 to the early phagosome. The recruitment of active Vps34 catalyzes the conversion of phosphatidylinositol phosphate to PtdIns(3)P, a key regulator of phagosomal maturation through the recruitment of EEA-1 and the production of reactive oxygen species by its recruitment of p40phox. Now, SLAM can connect the Gram-negative bacterial phagosome to antibacterial response.



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