title: ECM1 controls T(H)2 cell egress from lymph nodes through re-expression of S1P(1).
abstract: Type 2 helper T cells (T(H)2) are critically involved in allergies and asthma. Here we demonstrate that extracellular matrix protein-1 (ECM1) is highly and selectively expressed in T(H)2 cells. ECM1 deficiency caused impaired T(H)2 responses and reduced allergic airway inflammation in vivo. Functional analysis demonstrated that although the T(H)2 polarization of ECM1-deficient cells was unimpaired, these cells had a defect in migration and were retained in peripheral lymphoid organs. This was associated with reduced expression of KLF2 and S1P(1). We also found that ECM1 could directly bind the interleukin-2 (IL-2) receptor to inhibit IL-2 signaling and activate S1P(1) expression. Our data identify a previously unknown function of ECM1 in regulating T(H)2 cell migration through control of KLF2 and S1P(1) expression.
authors.affiliation: Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
authors.forename: Zhenhu
authors.initials: Z
authors.lastname: Li
authors.forename: Yuan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Zhiduo
authors.initials: Z
authors.lastname: Liu
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Wu
authors.forename: Yuhan
authors.initials: Y
authors.lastname: Zheng
authors.forename: Zhiyun
authors.initials: Z
authors.lastname: Tao
authors.forename: Kairui
authors.initials: K
authors.lastname: Mao
authors.forename: Jie
authors.initials: J
authors.lastname: Wang
authors.forename: Guomei
authors.initials: G
authors.lastname: Lin
authors.forename: Lin
authors.initials: L
authors.lastname: Tian
authors.forename: Yongyong
authors.initials: Y
authors.lastname: Ji
authors.forename: Meiling
authors.initials: M
authors.lastname: Qin
authors.forename: Shuhui
authors.initials: S
authors.lastname: Sun
authors.forename: Xueliang
authors.initials: X
authors.lastname: Zhu
authors.forename: Bing
authors.initials: B
authors.lastname: Sun
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D002454:Cell Differentiation / Q000235:genetics / Q000276:immunology; D002465:Cell Movement / Q000235:genetics / Q000276:immunology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D016326:Extracellular Matrix Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D008198:Lymph Nodes / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D016201:Receptors, Lymphocyte Homing / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D015398:Signal Transduction / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D019076:Transgenes / Q000235:genetics
chemical_list: C094556:Ecm1 protein, mouse; D016326:Extracellular Matrix Proteins; D009419:Nerve Tissue Proteins; D016201:Receptors, Lymphocyte Homing; C491561:Sip1 protein, mouse