Anti-tuberculosis treatment enhances the production of IL-22 through reducing the frequencies of regulatory B cell.

IL-22 has been suggested to play an important role in immune response against Mycobacterium tuberculosis infection. However, the exact role of IL-22 in human tuberculosis (TB) infection remains unclear and the regulatory mechanism of IL-22 response in human TB is unknown. In this study, we observed that successful anti-tuberculosis treatment induced an enhanced and sustained M. tuberculosis antigen-specific IL-22 response, correlated with the decrease of the frequencies of CD19(+)CD5(+)CD1d(+) regulatory B cells. We also found that depletion of CD19(+) B cells significantly enhanced M. tuberculosis antigen-specific IL-22 production by peripheral blood mononuclear cells. More importantly, we observed that purified CD19(+) B cells, and more efficiently, CD19(+)CD5(+)CD1d(+) regulatory B cells, suppressed IL-22 production. In summary, we showed here for the first time that effective anti-tuberculosis treatment restores M. tuberculosis antigen-specific IL-22 response through a novel mechanism by reducing the frequencies of CD19(+)CD5(+)CD1d(+) regulatory B cells in human TB.