Literature DB >> 21575994

CCR4 contributes to the pathogenesis of experimental autoimmune encephalomyelitis by regulating inflammatory macrophage function.

Eileen A Forde1, Rukiye-Nazan E Dogan, William J Karpus.   

Abstract

Chemokines and their receptors play a critical role in orchestrating the immune response during experimental autoimmune encephalomyelitis (EAE). Expression of CCR4 and its ligand CCL22 has been observed in ongoing disease. Here we describe a role for CCR4 in EAE, illustrating delayed and decreased disease incidence in CCR4(-/-) mice corresponding with diminished CNS infiltrate. Peripheral T cell responses were unaltered in CCR4(-/-) mice; rather, disease reduction was related to reduced CD11b(+)Ly6C(hi) inflammatory macrophage (iMϕ) numbers and function. These results provide evidence that CCR4 regulates EAE development and further supports the involvement of CCR4 in iMϕ effector function.
Copyright © 2011 Elsevier B.V. All rights reserved.

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Year:  2011        PMID： 21575994      PMCID： PMC3139027          DOI： 10.1016/j.jneuroim.2011.04.008

Source DB:  PubMed          Journal:  J Neuroimmunol        ISSN： 0165-5728            Impact factor:   3.478


  74 in total

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