1.
J Neuroimmunol
; 236(1-2): 17-26, 2011 Jul.
Artigo
em Inglês
| MEDLINE
| ID: mdl-21575994
RESUMO
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 (iMÏ) numbers and function. These results provide evidence that CCR4 regulates EAE development and further supports the involvement of CCR4 in iMÏ effector function.