Sema4D is required in both the adaptive and innate immune responses of contact hypersensitivity.pdfVIP

Sema4D is required in both the adaptive and innate immune responses of contact hypersensitivity.pdf

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Sema4D is required in both the adaptive and innate immune responses of contact hypersensitivity.pdf

S r Z C a b c a A R R A A K S C C A I 1 a d s h A e e ( i ( C h 0Molecular Immunology 78 (2016) 98–104 Contents lists available at ScienceDirect Molecular Immunology j ourna l ho me pa g e : www.elsev ier .com/ locate /mol imm ema4D is required in both the adaptive and innate immune esponses of contact hypersensitivity henlai Zhua,1, Yang Luob,c,1, Jinlei Yua, Jixin Gaoa, Yueqiang Zhanga, Chunying Xiaoa, hen Zhanga, Gang Wanga, Yufeng Liua, Meng Fua, Xu Yaob,c, Wei Lia,b,c,? Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi’an, Shaanxi 710032, PR China Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, Jiangsu 210042, PR China Jiangsu provincial Key Laboratory of Molecular Biology for Skin Diseases and STIs, PR China r t i c l e i n f o rticle history: eceived 12 July 2016 eceived in revised form 26 August 2016 ccepted 2 September 2016 vailable online 8 September 2016 eywords: emaphorin 4D ontact hypersensitivity D8+ T cells daptive immunity nnate immunity a b s t r a c t Originally recognized as a regulator of axon guidance in the nervous system, Semaphorin 4D (Sema4D, CD100) also participates in various immune responses and many immune-related diseases. However, whether Sema4D is involved in the pathogenesis of contact hypersensitivity (CHS) remains unclear. In this study, we explored the role of Sema4D in oxazolone-induced CHS using Sema4D knockout (KO) mice. We found that Sema4D KO mice developed attenuated CHS responses, as indicated by milder ear-swelling, lower expression of IL-1, IL-6, CXCL2 and CXCL5, and decreased recruitment of neutrophils, CD8+ T cells and CD4+ T cells. CHS was impaired in the wide type (WT) mice reconstituted with bone marrow from Sema4D KO mice, indicating that deletion of Sema4D gene in hematopoietic cells

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