TY - JOUR
T1 - Resolvin E1 inhibits dendritic cell migration in the skin and attenuates contact hypersensitivity responses
AU - Sawada, Yu
AU - Honda, Tetsuya
AU - Hanakawa, Sho
AU - Nakamizo, Satoshi
AU - Murata, Teruasa
AU - Ueharaguchi-Tanada, Yuri
AU - Ono, Sachiko
AU - Amano, Wataru
AU - Nakajima, Saeko
AU - Egawa, Gyohei
AU - Tanizaki, Hideaki
AU - Otsuka, Atsushi
AU - Kitoh, Akihiko
AU - Dainichi, Teruki
AU - Ogawa, Narihito
AU - Kobayashi, Yuichi
AU - Yokomizo, Takehiko
AU - Arita, Makoto
AU - Nakamura, Motonobu
AU - Miyachi, Yoshiki
AU - Kabashima, Kenji
N1 - Publisher Copyright:
© 2015 Sawada et al.
PY - 2015/10/19
Y1 - 2015/10/19
N2 - Resolvin E1 (RvE1) is a lipid mediator derived from ?3 polyunsaturated fatty acids that exerts potent antiinflammatory roles in several murine models. The antiinflammatory mechanism of RvE1 in acquired immune responses has been attributed to attenuation of cytokine production by dendritic cells (DCs). In this study, we newly investigated the effect of RvE1 on DC motility using two-photon microscopy in a contact hypersensitivity (CHS) model and found that RvE1 impaired DC motility in the skin. In addition, RvE1 attenuated T cell priming in the draining lymph nodes and effector T cell activation in the skin, which led to the reduced skin inflammation in CHS. In contrast, leukotriene B4 (LTB4) induced actin filament reorganization in DCs and increased DC motility by activating Cdc42 and Rac1 via BLT1, which was abrogated by RvE1. Collectively, our results suggest that RvE1 attenuates cutaneous acquired immune responses by inhibiting cutaneous DC motility, possibly through LTB4-BLT1 signaling blockade.
AB - Resolvin E1 (RvE1) is a lipid mediator derived from ?3 polyunsaturated fatty acids that exerts potent antiinflammatory roles in several murine models. The antiinflammatory mechanism of RvE1 in acquired immune responses has been attributed to attenuation of cytokine production by dendritic cells (DCs). In this study, we newly investigated the effect of RvE1 on DC motility using two-photon microscopy in a contact hypersensitivity (CHS) model and found that RvE1 impaired DC motility in the skin. In addition, RvE1 attenuated T cell priming in the draining lymph nodes and effector T cell activation in the skin, which led to the reduced skin inflammation in CHS. In contrast, leukotriene B4 (LTB4) induced actin filament reorganization in DCs and increased DC motility by activating Cdc42 and Rac1 via BLT1, which was abrogated by RvE1. Collectively, our results suggest that RvE1 attenuates cutaneous acquired immune responses by inhibiting cutaneous DC motility, possibly through LTB4-BLT1 signaling blockade.
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U2 - 10.1084/jem.20150381
DO - 10.1084/jem.20150381
M3 - Article
C2 - 26438363
AN - SCOPUS:84959894543
SN - 0022-1007
VL - 212
SP - 1921
EP - 1930
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
IS - 11
ER -