Multiple sclerosis (MS) is a chronic demyelinating autoimmune disease of the central nervous system (CNS) that is usually characterized by alternating periods of relapse and remission. The involvement of CD4+ helper T cells, especially the Th1 and Th17 subsets, during MS relapse is well established. However, recent reports suggest that there is plasticity and functional diversity of Th17 cells in CNS autoimmunity. Therefore, the overall picture of “encephalitogenic” T cells is difficult to draw. The chemokine system is fundamental for T cell trafficking, and plays essential roles in normal physiology and autoimmunity. Each Th subset expresses characteristic chemokine receptors that are critical for homing to inflammation sites. Chemokine receptor expression profiles on T cells in the cerebrospinal fluid (CSF) of MS patients reflect certain aspects of the pathology of MS relapse. Mounting evidence suggests that Th1- and Th17-related chemokines, and chemokine receptors mediate MS pathology. The scope of the present review was to discuss recent findings related to chemokine receptor expression and pathogenic Th cells in MS. This review focuses in particular on CCR2+CCR5+CCR6− Th1 cells, a newly identified Th cell subset that we recently showed is enriched in the CSF of relapsing MS patients. Measuring multiple chemokine receptor expression levels could show unique T cell subsets involved in the pathogenesis of various autoimmune diseases.