This immune response seems to significantly differ from the one developing during TBM, where granulomas are more rarely formed and persistent immune activation often leads to neuronal injury.32 Here, we demonstrated functionally divergent humoral profiles, characterized by highly functional and FcγR binding antibodies in pulmonary TB, in contrast to attenuated profiles in TBM with selective enrichment of cellular phagocytosis functions (ADCP). This evidence concerns the gene FCGR2A and meningeal tuberculosis.