回首頁 > 公告事項

公告事項 Announcements

6/6(四)Dr. I-hsin Su專題演講,請踴躍參加






講題:Talin1 controls TLR-mediated activation of dendritic cells through direct interaction with MyD88 and PIP5K
講者:I-hsin Su, Ph.D.

Associate Professor, School of Biological Sciences
Laboratory of Molecular Immunology & Cell Signaling
Nanyang Technological University Singapore

Talin critically controls integrin-dependent cell migration, but its regulatory role in skin dendritic cells (DCs) during inflammatory responses has not been investigated. Here we found that talin1 not only regulated integrin-dependent Langerhans cells (LCs) migration, but also MyD88-dependent toll-like receptor (TLR) stimulated DC activation. Talin1-deficient LCs failed to exit epidermis, resulting in reduced LC migration to skin-draining lymph nodes (sdLNs) and defective skin tolerance induction, whereas talin1-deficient dermal DCs were unexpectedly accumulated in the dermis albeit their actomyosin-dependent migratory capabilities. Talin1-deficient DCs exhibited compromised chemotaxis, NFкB activation and pro-inflammatory cytokine production. Mechanistically, talin1 was required for the formation of a pre-assembled TLR complex with TIRAP and MyD88 via interacting with MyD88/PIP5K, and the subsequent assembly of TLR signalosome upon stimulation but was dispensable for the MyD88-independent, TLR3-induced assembly of TRIF-complex. Thus, Talin1 regulates MyD88-dependent TLR signaling pathways in DCs through a novel mechanism with implications for antimicrobial and inflammatory immune responses.



相關下載 Download