AIM2 and Psoriasis

Abstract

Psoriasis is a chronic inflammatory skin disease occurring worldwide, with multiple systemic complications, which seriously affect the quality of life and physical and mental health of patients. The pathogenesis of psoriasis is related to the environment, genetics, epigenetics, and dysregulation of immune cells such as T cells, dendritic cells (DCs), and nonimmune cells such as keratinocytes. Absent in melanoma 2 (AIM2), a susceptibility gene locus for psoriasis, has been strongly linked to the genetic and epigenetic aspects of psoriasis and increased in expression in psoriatic keratinocytes. AIM2 was found to be activated in an inflammasome-dependent way to release IL-1β and IL-18 to mediate inflammation, and to participate in immune regulation in psoriasis, or in an inflammasome-independent way by regulating the function of regulatory T(Treg) cells or programming cell death in keratinocytes as well as controlling the proliferative state of different cells. AIM2 may also play a role in the recurrence of psoriasis by trained immunity. In this review, we will elaborate on the characteristics of AIM2 and how AIM2 mediates the development of psoriasis.

Clinicopathologic Overlap of Vulvar Psoriasis and Candidiasis

“…Long-lived and abundant in squamous epithelium, a subset of T RM cells locally produce psoriasis-associated cytokines IL-17A, IFN-γ, and IL-22. This tissue-localized inflammatory pathway may explain recurrence of psoriasis in the same location after withdrawal of biologic therapies 27 . The clinicopathologic and immunological overlap of psoriasis and candidiasis suggests a hypothesis that candidal antigens activate T RM cells, inducing the vulvar psoriasiform rash seen in candidiasis even when fungal elements are microscopically absent from affected skin.…”

Pyroptosis: a new insight into intestinal inflammation and cancer

“…AIM2 is a cytoplasmic dsDNA sensor and an ALR inflammasome sensor ( 38 ). Under normal conditions, AIM2 is autoinhibited.…”

Characteristics and sources of tissue-resident memory T cells in psoriasis relapse

“…CD49a − CD103 + CD8 + Trm cells secrete more IL-17 upon activation to contribute to psoriasis-like inflammation. Basal keratin-forming cells with stem cell properties present in skin lesions maintain memory capacity in inflammation by increasing Aim2 [ Zhang, Y., Xu, X., Cheng, H., Zhou, F. 2023 ]. Together, these factors contribute to uncontrolled KC proliferation/differentiation and persistent inflammation in psoriasis [ Bromley, S. K et al, 2020 ; Qin, Y., Gao, C., Luo, J.…”