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231224s2016 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2016.06.004
|2 doi
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|a pubmed25n0871.xml
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|a (DE-627)NLM261614983
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|a (NLM)27327113
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|a (PII)S1521-6616(16)30097-3
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Zheng, Peiguo
|e verfasserin
|4 aut
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| 245 |
1 |
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|a Antigen-oriented T cell migration contributes to myelin peptide induced-EAE and immune tolerance
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|c 2016
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 31.03.2017
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|a Date Revised 13.08.2017
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2016 Elsevier Inc. All rights reserved.
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|a Treatment with soluble myelin peptide can efficiently and specifically induce tolerance to demyelination autoimmune diseases including multiple sclerosis, however the mechanism underlying this therapeutic effect remains to be elucidated. In actively induced mouse model of experimental autoimmune encephalomyelitis (EAE) we analyzed T cell and innate immune cell responses in the central nervous system (CNS) and spleen after intraperitoneal (i.p.) infusion of myelin oligodendrocyte glycoprotein (MOG). We found that i.p. MOG infusion blocked effector T cell recruitment to the CNS and protected mice from EAE and lymphoid organ atrophy. Innate immune CD11b(+) cells preferentially recruited MOG-specific effector T cells, particularly when activated to become competent antigen presenting cells (APCs). During EAE development, mature APCs were enriched in the CNS rather than in the spleen, attracting effector T cells to the CNS. Increased myelin antigen exposure induced CNS-APC maturation, recruiting additional effector T cells to the CNS, causing symptoms of disease. MOG triggered functional maturation of splenic APCs. MOG presenting APCs interacted with MOG-specific T cells in the spleen, aggregating to cluster around CD11b(+) cells, and were trapped in the periphery. This process was MHC II dependent as an MHC II directed antibody blocked CD4(+) T cell cluster formation. These findings highlight the role of myelin peptide-loaded APCs in myelin peptide-induced EAE and immune tolerance
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Experimental autoimmune encephalomyelitis
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| 650 |
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|a Immune tolerance
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|a T-cell migration
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| 650 |
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|a Cytokines
|2 NLM
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| 650 |
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|a Myelin-Oligodendrocyte Glycoprotein
|2 NLM
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| 650 |
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|a Peptide Fragments
|2 NLM
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| 650 |
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|a myelin oligodendrocyte glycoprotein (35-55)
|2 NLM
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| 700 |
1 |
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|a Fu, Hanxiao
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wei, Gaohui
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wei, Zhongwei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhang, Junhua
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ma, Xuehan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Rui, Dong
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Meng, Xianchun
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ming, Liang
|e verfasserin
|4 aut
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| 773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 169(2016) vom: 12. Aug., Seite 36-46
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
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|g volume:169
|g year:2016
|g day:12
|g month:08
|g pages:36-46
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2016.06.004
|3 Volltext
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