CCR4 contributes to the pathogenesis of experimental autoimmune encephalomyelitis by regulating inflammatory
Eileen A Forde1, Rukiye-Nazan E Dogan, William J Karpus
1Department of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
None:
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.
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