Protein 4.1R attenuates autoreactivity in experimental autoimmune encephalomyelitis by suppressing CD4+ T cell activation

被引：6

作者：

Liu, Xin ^{[1
]}

Zhou, Qingqing ^{[1
]}

Ji, Zhenyu ^{[2
]}

Fu, Guo ^{[1
]}

Li, Yi ^{[1
]}

Zhang, Xiaobei ^{[3
]}

Shi, Xiaofang ^{[3
]}

Wang, Ting ^{[1
]}

Kang, Qiaozhen ^{[1
]}

机构：

[1] Zhengzhou Univ, Sch Life Sci, Zhengzhou 450001, Peoples R China

[2] Zhengzhou Univ, Henan Acad Med & Pharmaceut Sci, Zhengzhou 450052, Peoples R China

[3] Nanyang Pukang Pharmaceut Corp Ltd, Nanyang 473053, Peoples R China

来源：

CELLULAR IMMUNOLOGY | 2014年 / 292卷 / 1-2期

基金：

中国国家自然科学基金;

关键词：

Protein; 4.1R; Multiple sclerosis; Experimental autoimmune encephalomyelitis; CD4(+) T cell; Autoimmunity disease; IMMUNOLOGICAL-SYNAPSE; MULTIPLE-SCLEROSIS; CYTOSKELETON; PATHOGENESIS; ASSOCIATION; MODULATION; RECEPTOR; COMPLEX;

D O I：

10.1016/j.cellimm.2014.08.005

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Immune synapse components contribute to multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) pathogenesis as they play important role in autoreactive T cell activation. Protein 4.1R, a red cell membrane cytoskeletal protein, recently was identified as an important component of immunological synapse (IS) and acted as the negative regulator of CD4(+) T cell activation. However, the pathological role of 4.1R in the MS/EAE pathogenesis is still not elucidated. In this study, we investigated the potential role of protein 4.1R in pathologic processes of EAE by using 4.1R knockout mouse model. Our results suggest that 4.1R can prevent pathogenic autoimmunity in MS/EAE progression by suppressing the CD4(+) T cell activation. (C) 2014 Elsevier Inc. All rights reserved.

引用

页码：19 / 24

页数：6

共 41 条

[1] Association between myeloid malignancies and acquired deficit in protein 4.1R:: A retrospective analysis of six patients
Alanio-Brechot, Cecile
Schischmanoff, Pierre-Olivier
Feneant-Thibault, Madeleine
Cynober, Therese
Tchernia, Gil
Delaunay, Jean
Garcon, Loic
[J]. AMERICAN JOURNAL OF HEMATOLOGY, 2008, 83 (04) : 275 - 278
[2] RAGE potentiates Aβ-induced perturbation of neuronal function in transgenic mice
Arancio, O
Zhang, HP
Chen, X
Lin, C
Trinchese, F
Puzzo, D
Liu, SM
Hegde, A
Yan, SF
Stern, A
Luddy, JS
Lue, LF
Walker, DG
Roher, A
Buttini, M
Mucke, L
Li, WY
Schmidt, AM
Kindy, M
Hyslop, PA
Stern, DM
Du Yan, SS
[J]. EMBO JOURNAL, 2004, 23 (20) : 4096 - 4105
[3] Broux B, 2013, CRIT REV IMMUNOL, V33, P283
[4] Immune synapses in T-cell activation
Cemerski, Saso
Shaw, Andrey
[J]. CURRENT OPINION IN IMMUNOLOGY, 2006, 18 (03) : 298 - 304
[5] Protein 4.1R regulates cell adhesion, spreading, migration and motility of mouse keratinocytes by modulating surface expression of β1 integrin
Chen, Lixiang
Hughes, Richard A.
Baines, Anthony J.
Conboy, John
Mohandas, Narla
An, Xiuli
[J]. JOURNAL OF CELL SCIENCE, 2011, 124 (14) : 2478 - 2487
[6] The role of CD4 T cells in the pathogenesis of multiple sclerosis
Chitnis, Tanuja
[J]. NEUROBIOLOGY OF MULTIPLE SCLEROSIS, 2007, 79 : 43 - 72
[7] Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS)
Constantinescu, Cris S.
Farooqi, Nasr
O'Brien, Kate
Gran, Bruno
[J]. BRITISH JOURNAL OF PHARMACOLOGY, 2011, 164 (04) : 1079 - 1106
[8] The immunological synapse
Creusot, RJ
Mitchison, NA
Terazzini, NM
[J]. MOLECULAR IMMUNOLOGY, 2002, 38 (12-13) : 997 - 1002
[9] Membrane-cytoskeleton interactions during the formation of the immunological synapse and subsequent T-cell activation
Das, V
Nal, B
Roumier, A
Meas-Yedid, V
Zimmer, C
Olivo-Marin, JC
Roux, P
Ferrier, P
Dautry-Varsat, A
Alcover, A
[J]. IMMUNOLOGICAL REVIEWS, 2002, 189 : 123 - 135
[10] Induction of EAE in mice with recombinant human MOG, and treatment of EAE with a MOG peptide
Devaux, B
Enderlin, F
Wallner, B
Smilek, DE
[J]. JOURNAL OF NEUROIMMUNOLOGY, 1997, 75 (1-2) : 169 - 173

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