Our findings indicate changes in the HCMB immune response to mycobacterial antigens that could account for their improved resistance to developing leprosy, as follows: i) an increase in the frequencies of memory CD4 and CD8 T cells responsive to the M. leprae whole-cell sonicate; ii) higher frequencies of CD4+ T cells that recognize M. leprae-specific peptides; and iii) higher production levels of the inflammatory mediators IL1-β, IL-6, IL-17, TNF, IFN-γ, MIP1-β, and MCP-1 by PBMCs in response to mycobacterial antigens. The gene discussed is CCL4; the disease is leprosy.