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1
Psoriasis involves the IL-23/IL-17 axis, driven by Th17 cells and ILC3s, which produce cytokines that activate keratinocytes and sustain inflammation.
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2
Th17 cells are adaptive immune cells that maintain chronic inflammation, while ILC3s provide a rapid, innate source of IL-17 and IL-22.
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3
Crosstalk between Th17 cells and ILC3s creates a self-amplifying inflammatory loop in psoriatic lesions.
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4
Immunological tipping points, such as the transition from innate to adaptive immunity, regulate the balance between Th17 cells and ILC3s.
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5
ILC3s and Th17 cells compete for IL-2, influencing the differentiation of Tregs and the inflammatory response in psoriasis.