期刊
JOURNAL OF AUTOIMMUNITY
卷 19, 期 4, 页码 175-181出版社
ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
DOI: 10.1006/jaut.2002.0613
关键词
experimental autoimmune encephalomyelitis; chemokine; chemokine receptor; inflammatory cell trafficking; neuroinflammation
类别
资金
- FIC NIH HHS [1R03 TW00784] Funding Source: Medline
- NINDS NIH HHS [2R01 NS32151] Funding Source: Medline
- PHS HHS [P05A 07021] Funding Source: Medline
Chemokines are chemotactic cytokines, which stimulate migration of inflammatory cells towards tissue sites of inflammation. The largest chemokine group, termed CC chemokines (CCLs), act primarily on T cells and monocytes, through CC chemokine receptors (CCRs) belonging to the superfamily of G-protein coupled seven transmembrane domain receptors. CCR expression is a critical determinant of cellular responses to CCLs. In this report, we describe the expression pattern of mRNA encoding selected CCRs in the spinal cord and spleen of perfused and non-perfused mice at different stages of chronic-relapsing EAE (ChREAE). We detected increased expression of receptors (CCR1, CCR5) associated with T helper-1 (Th1) but not those (CCR3, CCR4) associated with Th2 T cells in spinal cord during initial attack and relapse of ChREAE. Expression of these CCRs correlated temporally and spatially with reported previously expression of corresponding CCLs. The principal cells expressing CCR5 were inflammatory cells invading the spinal cord. Our results supported the implication of Th1-associated CCRs in the CNS-specific inflammatory reaction of ChREAE. (C) 2002 Elsevier Science Ltd. All rights reserved.
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