期刊
IMMUNITY
卷 53, 期 5, 页码 1063-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2020.10.001
关键词
-
类别
资金
- NIH Shared Instrumentation Program [1S10OD012027-01A1, 1S10OD016372-01, 1S10RR020936-01, 1S10RR023440-01A1]
- NIH [K08AI121421, DP2AT009499, R01AI130019, T32HL116275, DFG PE2864/3-1, DK043351]
- Massachusetts General Hospital Transformative Scholar Award
- AAAAI Foundation
- Food Allergy Science Initiative
- Chan Zuckerberg Initiative
- Burroughs Wellcome Fund
- Harvard Stem Cell Institute
- Allergan Pharmaceuticals
Dendritic cells (DCs) of the cDC2 lineage initiate allergic immunity and in the dermis are marked by their expression of CD301b. CD301b(+) dermal DCs respond to allergens encountered in vivo, but not in vitro. This suggests that another cell in the dermis may sense allergens and relay that information to activate and induce the migration of CD301b(+) DCs to the draining lymph node (dLN). Using a model of cutaneous allergen exposure, we show that allergens directly activated TRPV1(+) sensory neurons leading to itch and pain behaviors. Allergen-activated sensory neurons released the neuropeptide Substance P, which stimulated proximally located CD301b(+) DCs through the Mas-related G-protein coupled receptor member A1 (MRGPRA1). Substance P induced CD301b(+) DC migration to the dLN where they initiated T helper-2 cell differentiation. Thus, sensory neurons act as primary sensors of allergens, linking exposure to activation of allergic-skewing DCs and the initiation of an allergic immune response.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据