Human immunodeficiency virus (HIV) and tuberculosis (TB) coinfection accounts for high rates of global morbidity and mortality. Although the pathogeneses of HIV and Mycobacterium tuberculosis (MTB) infections are different, the coexistence of both the agents will lead to accentuated disease progression in the host. Expression of markers associated with chronic immune activation, exhaustion, and immunosenescence on pathogen-specific CD4+ and CD8+ T cells have been associated with suboptimal immune responses in HIV–TB coinfection. The effect of chronic immune activation, exhaustion, and immunosenescence also appears to extend across distinct sets of immune cells, and hence a wider understanding of the mechanistic aspects underlying these phenomena is urgently required to necessitate the expansion of immune cells with improved functions in HIV–TB coinfection. Furthermore, strategies to cause attrition of immunosenescence and immune activation appear to stem from an improved understanding of senescence signaling.