Abstract: Experimental autoimmune encephalomyelitis (EAE) is a ThI-mediated autoimmune disease of the central nervous system that is widely used as an animal model of multiple sclerosis (MS). Herein it is demonstrated that CXCR2, a chemokine receptor involved in the recruitment of neutrophils, is expressed in tissues with EAE lesions. Blockade or deficiency of CXCR2 reduces the infiltration of neutrophils to sites of inflammation. Thus provided herein are reagents that antagonize or inhibit ELR+CXC chemokines and methods of use of these reagents in preventing and treating organ-specific autoimmune diseases like multiple sclerosis, and methods or treating various inflammatory conditions and diseases.