期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 192, 期 6, 页码 899-905出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.192.6.899
关键词
multiple sclerosis; experimental autoimmune encephalomyelitis; CC chemokine receptor 2; knockout; CCL2
资金
- NIAID NIH HHS [AI07476] Funding Source: Medline
- NINDS NIH HHS [NS34510] Funding Source: Medline
Experimental autoimmune encephalomyelitis (EAE) is a CD4(+) T lymphocyte-mediated disease of the central nervous system (CNS) characterized by mononuclear cell infiltration, demyelination, and paralysis. We previously demonstrated a role for chemokines in acute and relapsing EAE pathogenesis. Presently, we investigated the role of CC chemokine receptor 2 (CCR2) in acute EAE. CCR2(-/-) mice did not develop clinical EAE or CNS histopathology, and showed a significant reduction in T cell- and CNS-infiltrating CD45(high)F4/80(+) monocyte subpopulations. Peripheral lymphocytes from CCR2(-/-) mice produced comparable levels of interferon-gamma (IFN-gamma) and interleukin (IL)-2 in response to antigen-specific restimulation when compared with control mice. Adoptively transferred myelin oligodendrocyte glycoprotein 35-55-specific T cells lacking expression of CCR2 were able to induce EAE, whereas CCR2(-/-) recipients of wild-type T cells failed to develop disease. These results suggest that CCR2 expression on host-derived mononuclear cells is critical for disease induction.
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