(5) Given that CCL2 favors Th2 response which is evident from CCL2−/− mice that confer resistance against parasitic infection (22, 23) under this scenario, a higher CCL2 level in the BAL of HIV-1/Mtb patients (39) will generate a Th2 dominant environment that presumably suppresses Mtb-specific IFN-γ mediated Th1 immunity (Figure 1). This evidence concerns the gene CCL2 and parasitic infectious disease.