Antigen presentation in EAE: role of microglia, macrophages and dendritic cells

被引:108
作者
Almolda, Beatriz [1 ]
Gonzalez, Berta [1 ]
Castellano, Bernardo [1 ]
机构
[1] Univ Autonoma Barcelona, Unit Histol, Dept Cell Biol Physiol & Immunol, Inst Neurosci, Bellaterra 08193, Spain
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2011年 / 16卷
关键词
microglia; dendritic-cells; MHC; EAE; T-cell; neuroimmunology; tolerance; CNS; Review; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; REGULATORY T-CELLS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; ACTIN-BUNDLING PROTEIN; FUNCTION IN-VIVO; RAT SPINAL-CORD; MULTIPLE-SCLEROSIS; IMMUNE-RESPONSES; DEMYELINATING DISEASE;
D O I
10.2741/3781
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Experimental autoimmune encephalomyelitis (EAE), a well-established model of multiple sclerosis, is characterised by microglial activation and lymphocytic infiltration. Lymphocytic activation through the antigen presentation process involves three main signals, the first provided by the engagement of major histocompatibility complex molecules (MHC) with the receptor of T-cells (TCR), the second by the binding of co-stimulatory molecules and the third by the secretion or expression of T-cell polarising molecules in specific populations of antigen presenting cells (APC). Microglial cells are considered to be the main APC population in the central nervous system (CNS). Specifically in EAE an increase in MHCs, costimulatory molecules and different T-cell polarising factors have been reported in microglia. However, a growing number of evidences suggest that dendritic cells (DCs), the main APC in the peripheral immune system, may also participate in the regulation of T-cell responses within the CNS. In this review we summarize the principal knowledge regarding microglial/macrophage function in EAE and their role in T-cell modulation, as well as the participation of DCs in the immune response associated to this disease.
引用
收藏
页码:1157 / 1171
页数:15
相关论文
共 178 条
[91]   Understanding the mechanisms of sustained signaling and T cell activation [J].
Lanzavecchia, A .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (10) :1717-1719
[92]   TURNOVER OF RESIDENT MICROGLIA IN THE NORMAL ADULT-MOUSE BRAIN [J].
LAWSON, LJ ;
PERRY, VH ;
GORDON, S .
NEUROSCIENCE, 1992, 48 (02) :405-415
[93]   Regional and temporal expression patterns of interleukin-10, interleukin-10 receptor and adhesion molecules in the rat spinal cord during chronic relapsing EAE [J].
Ledeboer, A ;
Wierinckx, A ;
Bol, JGJM ;
Floris, S ;
de Lavalette, CR ;
De Vries, HE ;
van den Berg, TK ;
Dijkstra, CD ;
Tilders, FJH ;
Van Dam, AM .
JOURNAL OF NEUROIMMUNOLOGY, 2003, 136 (1-2) :94-103
[94]   Molecular basis of T cell inactivation by CTLA-4 [J].
Lee, KM ;
Chuang, E ;
Griffin, M ;
Khattri, R ;
Hong, DK ;
Zhang, WG ;
Straus, D ;
Samelson, LE ;
Thompson, CB ;
Bluestone, JA .
SCIENCE, 1998, 282 (5397) :2263-2266
[95]   CD28/B7 system of T cell costimulation [J].
Lenschow, DJ ;
Walunas, TL ;
Bluestone, JA .
ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 :233-258
[96]   Regulation of PD-1, PD-L1, and PD-L2 expression during normal and autoimmune responses [J].
Liang, SC ;
Latchman, YE ;
Buhlmann, JE ;
Tomczak, MF ;
Horwitz, BH ;
Freeman, GJ ;
Sharpe, AH .
EUROPEAN JOURNAL OF IMMUNOLOGY, 2003, 33 (10) :2706-2716
[97]   COMPETITIVE PCR QUANTIFICATION OF CD4, CD8, ICAM-1, VCAM-1, AND MHC CLASS-II MESSENGER-RNA IN THE CENTRAL-NERVOUS-SYSTEM DURING DEVELOPMENT AND RESOLUTION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS [J].
LINDSEY, JW ;
STEINMAN, L .
JOURNAL OF NEUROIMMUNOLOGY, 1993, 48 (02) :227-234
[98]   USE OF CARBON LABELING TO DEMONSTRATE THE ROLE OF BLOOD MONOCYTES AS PRECURSORS OF THE AMEBOID CELLS PRESENT IN THE CORPUS-CALLOSUM OF POSTNATAL RATS [J].
LING, EA ;
PENNEY, D ;
LEBLOND, CP .
JOURNAL OF COMPARATIVE NEUROLOGY, 1980, 193 (03) :631-657
[99]  
LING EA, 1979, J ANAT, V128, P847
[100]   THE ORIGIN AND NATURE OF RAMIFIED AND AMEBOID MICROGLIA - A HISTORICAL REVIEW AND CURRENT CONCEPTS [J].
LING, EA ;
WONG, WC .
GLIA, 1993, 7 (01) :9-18