Importantly, simultaneous PD-1 blockage and co-stimulation through SLAMF1 increased the IFN-γ secreted by cells from pleural fluids and peripheral blood in LR TB patients (subjects with the non-responder endotype) up to the levels produced by HR individuals (individuals with the responder endotype), demonstrating the relevance of the balance between costimulatory molecules and checkpoint proteins in determining the anti-TB host response. Here, SLAMF1 is linked to tuberculosis.