FCGR1A and tuberculosis: Due to an improved control of Mtb in FCGR1-knockout mice [49] and a decrease in FCGR1A concentrations after anti-tuberculosis treatment in humans [48], we hypothesized that soluble FCGR1A had a negative impact on the immune response to MAP and facilitated their intracellular survival by interacting with soluble immune complexes and blocking Fc-dependent immune reactions [55].