IMMUNE-MEDIATED PATHOGENETIC MECHANISMS OF ATOPIC DERMATITIS IN CHILDREN

Authors

  • Sobirjonova Shakhzodakhon Gofforjon kizi Fergana Medical Institute of Public Health Assistant of the Department of Dermatovenereology and Allergology

Keywords:

atopic dermatitis, Th2 lymphocytes, interleukin-4, interleukin-13, IgE hypersensitivity, type 2 innate lymphoid cells, TSLP alarmin, filaggrin deficiency, eosinophilia, JAK/STAT pathway, Staphylococcus aureus colonization, IL-31 pruritus, SCORAD index, epidermal differentiation complex, pediatric immunology

Abstract

Atopic dermatitis (AD) affects up to 20% of children globally and is the most prevalent chronic inflammatory skin disease in pediatric populations. Its pathogenesis is governed by a bidirectional interaction between innate and adaptive immune dysfunction: keratinocyte-derived alarmins (TSLP, IL-33, IL-25) prime type 2 innate lymphoid cells and Th2 lymphocytes, which produce IL-4, IL-13, IL-31, and IL-5, driving IgE class switching, eosinophilia, barrier disruption, and neurogenic pruritus through JAK1-mediated signaling cascades.

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Published

2026-05-06

Issue

Vol. 4 No. 5 (2026): WOM

Section

Articles

License

Creative Commons License

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

How to Cite

IMMUNE-MEDIATED PATHOGENETIC MECHANISMS OF ATOPIC DERMATITIS IN CHILDREN. (2026). Web of Medicine: Journal of Medicine, Practice and Nursing , 4(5), 70-76. https://webofjournals.com/index.php/5/article/view/6343