c infection due to prolonged administration of corticosteroids to suppress pneumonitis ([@B19]). However, a report by Lee et al. in 2016 ([@B7]), subsequently confirmed by others ([@B8]--[@B15]), alerted clinical oncologists to the existence of alternative mechanisms of anti-PD-1-therapy-related development of acute PTB. In contrast to opportunistic infection with *M. tuberculosis*, these alternative mechanisms appear to involve triggering of exuberant, harmful pulmonary inflammatory responses due to reactivation of immune responsiveness to latent *M. tuberculosis* bacilli.

With respect to immunopathogenesis, Barber et al. in their recent description of two cases of PD-1 blockade-associated PTB, also reported that administration of the immune checkpoint inhibitor resulted in an increased prevalence of circulating *M. tuberculosis*-specific, interferon-γ (IFN-γ)-producing CD4 Th1 cells, but not Th17 cells, CD8 cells, regulatory T cells, or specific antibodies ([@B14]). These findings in humans are in agreement with several earlier studies in which CD4 T cell PD-1 gene knockout mice were used to investigate the role of this immune checkpoint inhibitor in the immunopathogenesis of acute, pulmonary *M. tuberculosis* infection ([@B25]--[@B27]). In these experimental animal studies, deficiency of PD-1 was found to result in excessive production of IFN-γ in the lungs of *M. tuberculosis*-infected mice, which, as opposed to controlling the infection, resulted in increased pulmonary bacterial loads, lung pathology and mortality, clearly underscoring a role for PD-1 in regulating harmful IFN-γ-mediated lung inflammation and dysfunction ([@B25]--[@B27]). However, as noted by Barber et al., further studies in the clinical setting are necessary to establish the exact mechanisms involved in PD-1-targeted therapy-related development of acute PTB ([@B14]).

Nevertheless, it is noteworthy in this context, that IFN-γ has been reported to suppress expression of the macrophage class-A scavenger receptor known as macrophage rec