AGE, AUTOIMMUNITY, AND INFLAMMATION: THE CURIOUS CASE OF IMMUNOSENESCENCE AND INFLAMM-AGING

An ever-aging population has caused an increase in the prevalence of diseases which occur in the elderly like diabetes and cancer; and autoimmune disease like rheumatoid arthritis (RA). On the other hand, ageing also causes an increased susceptibility to infections, reactivation of latent infections and a poorer vaccine response. Together, this ageing-related decline in immunity is called immunosenescence and the associated ageing-related inflammation is called inflamm-aging. In this brief review, we describe the changes seen with ageing in innate and adaptive immunity and how these lead to the various peculiarities associated with ageing in the immune system. TEMRA cells, Senescence associated secretory phenotype (SASP) and exhausted T cells are the main changes that occur in ageing T cells. Age-associated B cells (ABCs) contribute to changes associated with autoimmunity in elderly. In the innate arm, the macrophages-led inflamm-aging cause an overall net pro-inflammatory state. However, the macrophages have reduced phagocytosis leading to accumulation of necrotic and apoptotic debris. We also attempt to explain how immunosenescence and inflamm-aging cause defective vaccine responses and an increased predisposition to autoimmune diseases. As the average life expectancy of the world continues to increase, this is not just a curiosity to study at whim, but an indispensable part of medicine in the near-future.