Surprisingly, although treatment with TAK779 (a CXCR3 and CCR5 antagonist), anti-CCL5 mAb, AMD3100 (inhibits CXCL12) and Pertussis toxin (PTX; inhibitor of all Gi protein coupled chemokine receptors) all significantly suppressed the chemotaxis of infection-derived, WSX-1−/−, CD4+ T cells towards the respective recombinant chemokines (Fig. 3A, B), none of these inhibitors prevented the migration of the purified CD4+ T cells towards infection-derived, WSX-1−/− or WT, liver cells (Fig. 3C and results not shown for WT liver cells). The gene discussed is CXCR3; the disease is infection.