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This research suggests that innate lymphoid cells type 1 (ILC1) may contribute to the development of alopecia areata, alongside CD8+ T cells, by disrupting hair follicle immune privilege and promoting features of the disease.

In this study, researchers found that the cell surface protein Lrig1 plays a crucial role in regulating the suppressive function of regulatory T cells, suggesting it as a potential target for treating autoimmune diseases, as evidenced by experiments in mouse models.

This study found that ILC1-like cells can induce alopecia areata in healthy human hair follicles, challenging the traditional belief that the disease is primarily driven by CD8+ T cells.

In this study, researchers reported that IL-17C plays a key pro-inflammatory role in human skin diseases and may be a promising therapeutic target for inflammatory skin conditions.

Interleukin-1β stops hair growth by increasing cyclic AMP levels.

This study suggests that rather than inhibiting IL-15, selectively stimulating IL-15Ra-mediated signaling could be beneficial for managing alopecia areata and possibly other inflammatory hair loss conditions, as IL-15 promoted hair growth and maintained immune privilege in human hair follicles.

This study found that IL18 signaling plays a crucial role in the homing and retention of mature regulatory T cells in the mouse thymus, primarily by upregulating the chemokine receptor CCR6.

This study reported that IL-15 promotes human hair growth and protects hair follicle immune privilege, potentially stabilizing alopecia areata treatment outcomes when selectively stimulating IL-15Rα signaling.

This study found that ILC1-like cells can induce alopecia areata in healthy human hair follicles, suggesting that these cells might be a therapeutic target in AA management.

This study indicates that innate lymphoid cells-type 1 may provoke alopecia areata by disrupting hair follicle immune privilege and inducing characteristic lesions, challenging the view that alopecia areata is purely an autoantigen-dependent, T cell-driven condition.

This study provides evidence that innate lymphoid cells-type 1 can induce alopecia areata in human hair follicles, challenging the view that it is solely a CD8+ T cell-driven autoimmune disease.

This study suggests that interleukin-15 plays a complex role in alopecia areata, potentially contributing to immune infiltration while also protecting against hair follicle immune privilege collapse and promoting hair growth.

This study found that DC-HIL+ myeloid derived suppressor cells are increased in the blood and skin of patients with cutaneous lupus erythematosus and show immunosuppressive properties.

This study found elevated levels of IL-18 and free IL-18 in hidradenitis suppurativa patients compared to healthy controls, suggesting these cytokines may serve as novel biomarkers for disease activity, with correlations indicating their involvement in disease severity.

This study suggests that IL-1β produced by dermal papilla cells, regulated by protein kinase C, may inhibit human hair follicle growth through paracrine signaling.

This study found that rhIL-15 promotes human hair follicle growth and regrowth in experimental settings and may have therapeutic potential for alopecia areata by restoring immune privilege guardianship.

This study suggests that interleukin-1 α influences dermal papilla cell activity by modifying androgen receptor expression and increasing the secretion of several growth factors and cytokines.

ASLAN004 was safe and well-tolerated, supporting further development for treating certain diseases.

In this study, researchers found that the rs3118470 mutation in the IL2RA gene significantly increases the risk of developing alopecia areata, and they emphasize the need for future research with larger, more diverse populations to validate these results.

This study found that in immunodeficient mice lacking T cells, certain innate lymphoid cell subsets increased and influenced the hair growth cycle, with specific ILC subsets shown to promote anagen, the active phase of hair growth.

This study suggests that in alopecia areata, innate lymphoid cells type 1 may contribute to the disease’s pathogenesis by inducing hair follicle changes similarly to CD8+ T cells.

This article reviews the role of IL-17 in inflammatory skin disorders and highlights its potential therapeutic targeting in both neutrophilic and lymphocyte-mediated conditions, reporting no new experimental results.

This study discovered that DNA damage independently induces IL-19 and IL-24 cytokines, which regulate senescence-associated secretory phenotype factors, suggesting potential pathways for treating cancer and age-related diseases.

RNase L suppresses regeneration in mammals.

This study found that blocking LFA-1 signaling completely prevented the development of alopecia areata in C3H/HeJ mice, suggesting that LFA-1 plays a crucial role in the disease's pathogenesis and could be a target for new therapies.

In this study, researchers observed that dysregulated innate lymphoid cells type 1, alongside CD8+ T cells, may contribute to the pathogenesis of alopecia areata by affecting hair follicle health.

IL-13 protein is much higher in the skin of atopic dermatitis patients than in healthy skin.

This review highlights recent insights into how IL-15 influences T cell responses and contributes to immunopathogenesis in various diseases, suggesting its crucial role in TCR-independent activation and potential in optimizing therapeutic strategies.

This study found that patients with alopecia areata had significantly higher serum IL-1R1 levels, IL-1R1 gene expression, and hsa-miR-19b-3p levels compared to healthy controls, suggesting these could serve as diagnostic and prognostic markers for the disease's severity.

This study found that innate lymphoid cells-type 1 (ILC1lc) can induce alopecia areata (AA) by disrupting hair follicle immune privilege and causing hair follicle dystrophy and regression in both ex vivo and in vivo settings.