Aging is a biological aspect of human physiological development. Age-associated changes or immunosenescence in the immune cell population, phenotype, and functions are associated with the risk of several diseases and infections. Immunosenescence in aging skin is believed to be related to decreased protective immunity, auto inflammation and autoimmunity, reduced vaccine efficacy, and impaired tolerance nature to harmless antigens. Several phenomena responsible for aging include telomere shortening, reactive oxidative species (ROS) formation, DNA damage, production of the senescence-associated secretory phenotype (SASP), and inflammaging. In the skin, decreased innate response and adaptive capability were observed. With aging, Langerhans cells (LCs)’ ability to migrate to lymph nodes was decreased, neutrophils’ activation, recognition ability, phagocytosis was diminished coupled with defective chemotaxis, dendritic cells (DCs)’ antigen presentation response was dysfunctional, and monocytes/macrophages have a respiratory burst disorder. In contrast, increased natural killer (NK) cells with decreased chemokine (interleukin [IL]-2 and IL-12) production as well as a retained production of antimicrobial peptides (AMPs) were reported. Impairment of B cells was also recognized, resulting in low-affinity antibody production against an antigen, while T cells revealed changes in the CD4 and CD8 function and Th17/Treg ratio changes leading to an imbalance between pro- and anti-inflammatory immune responses. In an attempt to slow the progression of immunosenescence, several strategies were developed, such as thymus reconstitution, reduction of antigenic stimulation, exogenous IL-2, dietary restrictions, probiotics, and vaccination.