Visceral fat tissue produces chronic inflammation through its interactions with the immune system. Numerous mechanisms are involved: generation of additional senescent cells and their inflammatory signaling; normal fat cells secreting signals similar to those of infected cells; DNA debris from dead fat cells; and others. In younger individuals, problematic inflammation arises through having too much fat tissue, being overweight or obese. In older individuals, however, many of the same problems of chronic inflammation arise even given lesser amounts of visceral fat tissue. This paper reviews some of the relevant mechanisms, comparing aging with obesity, looking for the differences under the hood in T cell behavior.
Basic aging mechanisms such as cellular senescence and diminished number or dysfunction of immune progenitor cells are causative factors of development of low-grade inflammation. Immunosenescence is a term to describe the decline of immune function associated with aging, which can lead to increased susceptibility to infections, cancer, and metabolic and autoimmune disorders. During the state of infection or tissue damage in healthy young individuals, the immune system moves quickly. After the effective removal of the invading pathogen, the host immune response must be deactivated and return to a quiescent state to prevent further tissue damage. A subset of T lymphocytes called regulatory T cells are responsible for suppressing the deleterious effects of immune response.
In general, both innate and adaptive immune systems are affected by aging, but adaptive immunity, especially T lymphocytes, are most susceptible to the detrimental effects of aging. Gradual deterioration of the immune system over the course of time leads to a mismatch between proinflammatory and anti-inflammatory signals that may disrupt inflammatory homeostasis causing inflammaging.
Inflammation in adipose tissue, mainly evidenced by increased accumulation and proinflammatory polarization of T cells and macrophages, has been well-documented in obesity and may contribute to the associated metabolic dysfunctions including insulin resistance. Studies show that increased inflammation, including inflammation in adipose tissue, also occurs in aging. Aging-associated inflammation in adipose tissue has some similarities but also differences compared to obesity-related inflammation. In particular, conventional T cells are elevated in adipose tissue in both obesity and aging and have been implicated in metabolic functions in obesity.
However, the changes and also possibly functions of regulatory T cells in adipose tissue are different in aging and obesity. In this review, we summarize recent advances in research on the changes of these immune cells in adipose tissue with aging and obesity and discuss their possible contributions to metabolism and the potential of these immune cells as novel therapeutic targets for prevention and treatment of metabolic diseases associated with aging or obesity.