THE ROLE OF INNATE LYMPHOID CELLS IN THE PATHOGENESIS OF PSORIASIS

Litus I. O., Kaidashev I. P.

THE ROLE OF INNATE LYMPHOID CELLS IN THE PATHOGENESIS OF PSORIASIS


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About the author:

Litus I. O., Kaidashev I. P.

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LITERATURE REVIEWS

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Scientific article

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Psoriasis is a chronic immune-mediated inflammatory skin disease in which, alongside cells of the adaptive immune system, innate immune mechanisms play an important role in its pathogenesis. Of particular interest are innate lymphoid cells (ILCs), which contribute to the maintenance of tissue homeostasis and barrier immune responses and are capable of rapidly responding to signals derived from epithelial, stromal, and myeloid cells. Unlike T lymphocytes, their activation does not require specific antigen recognition, enabling ILCs to rapidly participate in local immune responses. The aim of this study was to summarize and systematize current scientific evidence on the phenotypic and functional characteristics of the major ILC subsets and to determine their role in the immunopathogenesis of psoriasis. A narrative review of the scientific literature was conducted, including an analysis of experimental and clinical studies as well as review articles addressing ILC1, ILC2, and ILC3, their activation mechanisms, cytokine activity, tissue distribution, and plasticity, as well as the chemokine-mediated mechanisms involved in the recruitment of these cells to sites of psoriatic inflammation. Analysis of the available evidence demonstrated that individual ILC subsets exhibit distinct transcriptional and cytokine profiles that determine their functional specialization. ILC1 and natural killer (NK) cells are predominantly associated with type 1 immune responses and interferon gamma (IFN-γ) production, whereas ILC2 are characterized by the expression of GATA3 and the production of type 2 cytokines, including interleukin (IL)-4, IL-5, IL-9, and IL-13. ILC3 are distinguished by the expression of RORγt and their capacity to produce IL-17A and IL-22. The phenotypic composition of ILC populations varies according to their localization within different layers of the skin, while the inherent plasticity of these cells may further modulate their functional activity. The most compelling evidence for a pathogenetic role in psoriasis has been reported for ILC3. Their numbers are increased in the peripheral blood and skin of patients with psoriasis compared with healthy individuals and decrease during disease remission. ILC3 represent an important source of IL-17 and IL-22, while the IL-23–ILC3–IL-17/IL-22 axis is considered one of the mechanisms contributing to the maintenance of chronic inflammation and epidermal hyperplasia. Experimental evidence also supports the functional involvement of ILC3 in the development of psoriasis- like inflammation. An additional mechanism of potential importance is ILC2 plasticity, involving the acquisition of an ILC3-like phenotype and the capacity to produce IL-17. Thus, ILCs constitute an important component of the immunopathogenesis of psoriasis, with ILC3 exhibiting the most prominent pathogenetic significance among the major ILC subsets. Further elucidation of the mechanisms governing their activation, inhibition, plasticity, and migration, their interactions with keratinocytes and other cells of the innate and adaptive immune systems, as well as determination of the relative contributions of ILC3 and T helper 17 (Th17) cells to psoriatic inflammation, represents a promising direction for future research.

Tags:

immune cells, innate lymphoid cells, interleukins, keratinocytes, psoriasis, skin, tumor necrosis factor

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Publication of the article:

«Bulletin of problems biology and medicine», 2026 Issue 3, 182, 81-92 pages, index UDC 611.42-018.1:612.017.11:616.517-092

DOI:

10.29254/2077-4214-2026-3-182-81-92

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