Cellular Senescence in Immunity against Infections

Cellular senescence is characterized by irreversible cell cycle arrest in response to different triggers and an inflammatory secretome. Although originally described in fibroblasts and cell types of solid organs, cellular senescence affects most tissues with advancing age, including the lymphoid tissue, causing chronic inflammation and dysregulation of both innate and adaptive immune functions. Besides its normal occurrence, persistent microbial challenge or pathogenic microorganisms might also accelerate the activation of cellular aging, inducing the premature senescence of immune cells. Therapeutic strategies counteracting the detrimental effects of cellular senescence are being developed. Their application to target immune cells might have the potential to improve immune dysfunctions during aging and reduce the age-dependent susceptibility to infections. In this review, we discuss how immune senescence influences the host's ability to resolve more common infections in the elderly and detail the different markers proposed to identify such senescent cells; the mechanisms by which infectious agents increase the extent of immune senescence are also reviewed. Finally, available senescence therapeutics are discussed in the context of their effects on immunity and against infections.

Automated summary

Cellular senescence is an irreversible cell cycle arrest and inflammatory secretion phenomenon that affects various tissues, including lymphoid tissue, leading to chronic inflammation and immune dysfunction. Persistent microbial challenge or pathogenic microorganisms may accelerate cellular aging and premature senescence of immune cells. Therapeutic strategies targeting cellular senescence may improve immune dysfunctions in the elderly and reduce susceptibility to infections.