Abstract
Skin-resident stromal cells, including keratinocytes, fibroblasts, adipocytes, and immune cells including Langerhans cells, dendritic cells, T cells, and innate lymphoid cells, and their functional products work in concert to ensure the realization of skin barrier immunity. However, aging-induced immunosenescence predisposes the elderly to pruritic dermatoses, including type 2 inflammation-mediated. Inflammaging, characterized by chronic low level of pro-inflammatory cytokines released from senescent cells with the senescence-associated secretory phenotype (SASP), may drive immunosenescence and tangle with type 2 inflammatory dermatoses. The present mini-review summarizes current evidence on immunosenescence and type 2 inflammation in the skin and further focuses on future needs from an inflammaging perspective to clarify their complexity.
Highlights
The skin is the largest active immune organ, covering the body’s outermost layer and performing the function of resisting external stimulus, maintaining skin homeostasis
The current mini-review focuses on skin immunosenescence and type 2 inflammation and present future needs from an inflammaging perspective, promising better management of type 2 inflammatory dermatosis in the elderly (Figure 1)
The cells mentioned above work synergistically or antagonistically upon harmful environmental exposures challenge, leading to reinforced or compromised networks protecting the skin against damage or causing dermatosis, respectively
Summary
The skin is the largest active immune organ, covering the body’s outermost layer and performing the function of resisting external stimulus, maintaining skin homeostasis. Skin barrier inevitably undergoes characteristically immunological declines with advancing age, termed skin immunosenescence. Higher incidences of many dermatoses such as infectious diseases, noncommunicable autoimmune diseases, and cutaneous malignancies, and more pathological states such as unspecific itchiness and delayed wound healing are observed in the elderly alongside immunosenescence (Farage et al, 2009). Type 2 inflammatory dermatosis such as atopic dermatitis (AD), chronic spontaneous urticaria (CSU), and bullous pemphigoid (BP) frequently affect the elderly and are presumed to be correlated with skin immunosenescence. The diseases affecting the elderly are prone to more severity, therapeutic resistance, and longer duration. The current mini-review focuses on skin immunosenescence and type 2 inflammation and present future needs from an inflammaging perspective, promising better management of type 2 inflammatory dermatosis in the elderly (Figure 1)
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