Abstract

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.

Author Keywords: experimental autoimmune encephalomyelitis, chemokine, chemokine receptor, inflammatory cell trafficking, neuroinflammation