May 20th, 2026
Far too little research into infectious disease and the development of vaccines and other approaches to therapy employs old animals. It is accepted that infectious disease becomes worse with age and treatments become less effective, and then left to the smaller aging research community to see if anything can be done about it. Here, for example, is an example of research in which scientists attempt to build an incrementally better picture as to what exactly is going wrong in the aging immune system, in the specific context of a single infectious disease, tuberculosis. Matters move slowly.
Aging profoundly impairs immune competence, a phenomenon termed immunosenescence, rendering older adults (≥60 years) highly vulnerable to infectious diseases such as tuberculosis (TB). Clinically, older adults exhibit reduced vaccine effectiveness alongside heightened susceptibility to TB, with epidemiological data indicating 2-3 times higher TB incidence and up to four times higher mortality than younger patients. Despite this growing burden, current TB research predominantly employs young adult mouse models (6-8 weeks old, equivalent to ~18-year-old humans), which do not adequately capture the immune landscape of older hosts. Evidence from studies suggests that old mice exhibit higher bacterial burden, delayed CD4+ T cell responses, and altered immune activation compared to younger counterparts. However, the impact of immunosenescence on bacterial clearance dynamics, immune cell phenotypes, and host responses during TB treatment remain largely unexplored.
