There is a strong correlation between the decline of the immune system and a decrease in future lifespan. As the immune system performs a myriad of functions with a multitude of specialized cell types, its breakdown has serious ramifications for health and longevity. As we age, our immune systems steadily decline, becoming less efficient and more inclined to contribute to chronic inflammation due to inappropriate activation.
This smoldering chronic inflammation, also known as inflammaging, speeds up the development of various age-related diseases due to the crosstalk it has with the various damages of aging. In many ways, inflammaging is the glue that binds these damages together, as each of them has an inflammatory component and their progress is often accelerated in the presence of increased inflammation.
At a basic level, inflammation disrupts tissue maintenance and regeneration by blocking various repair pathways, so when that inflammation is chronic, as is commonly seen in aged individuals, the healing of organs and tissues is poor. Therefore, it is no surprise that chronic inflammation causes most older people to struggle to heal and recover from injury.
Why the immune system declines is not yet fully understood, but one reason appears to be an ever-increasing infectious burden caused by constant exposure to environmental pathogens. Some invaders, such as cytomegalovirus and other herpesviruses, evade the immune system and continue to spread over time, which ties up ever-increasing numbers of immune cells to try to slow down their spread.
The thymus, which produces the majority of our T cells, begins to shrink from a young age, and the number of replacement cells that it makes dwindles as we age. This process is called thymic involution, which also causes the immune system to decline. The immunological model of cancer shows increased cancer risk with the decline of the immune system, and thymic involution is a critical part of this increased risk.
An emerging hypothesis for age-related immune system decline is the role played by microbial burden and the increased permeability of the gut membrane. Some researchers even suggest that changes to the microbiome and a compromised gut membrane that drives increased microbial burden could be the origins of inflammaging.
Finally, immune cells themselves can become senescence associated due to exposure to the senescence-associated secretory phenotype (SASP), the pro-inflammatory signals that are given off by damaged senescent cells. It is possible for otherwise functional immune cells, such as macrophages and T cells, to become dysfunctional due to high inflammatory exposure, and they can begin to behave in a harmful manner and themselves contribute to the inflammation.
With this in mind, we want to highlight a study that looks at the relationship between longevity and immune function.
An increasing amount of data implicate immunity-mostly innate immunity-in the ageing process; both during healthy ageing as well as in neurodegenerative diseases. Despite the aetiology however, the underlying mechanisms are poorly understood. Here we review what we know from model organisms (worms, flies and mice) on the possible mechanistic details that connect immunity and ageing. These links provide evidence that inter-tissue communication (especially the interaction between gut and brain), hormonal control mechanisms and intestinal microbiota determine immune system activity and thus influence lifespan.
There is little doubt that the immune system plays a key role in longevity, and fully understanding why it breaks down and ways in which we can repair and improve its activity are critically important in the mission to end age-related diseases.
 Xia, J., Gravato-Nobre, M., & Ligoxygakis, P. (2019). Convergence of longevity and immunity: lessons from animal models. Biogerontology, 1-8.