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This study found that RNase L acts as a regeneration repressor gene in mammals, as seen in Rnasel-/- mice which showed increased regenerative capacity and elevated Wound Induced Hair Neogenesis through enhanced IL-36α signaling, suggesting a tradeoff between regeneration and immune regulation.

In this study, researchers identified IL18R+ thymus-resident regulatory T cells in mice, demonstrating their unique molecular features and resistance to age- and stress-induced thymus involution, highlighting IL18 signaling's role in Treg migration and retention.

This study suggests that IL-4 and IL-13 may play a role in the immunopathogenesis of alopecia areata in some patients, indicating a possible Th2-driven pathway in this condition.

This study found that ILC1-like cells can induce alopecia areata symptoms in both ex vivo human hair follicles and in vivo mouse models, challenging the view that alopecia areata is solely CD8+ T cell-driven.

This study found that recombinant murine IL-36α increased the number of regenerated hair follicles and accelerated wound healing in a mouse model of wound-induced hair follicle neogenesis.

This review examines the role of innate lymphoid cells in allergic diseases and the influence of an allergic microenvironment on their plasticity, without reporting new clinical outcomes.

This study suggests that IL-33 promotes hair follicle changes and T cell infiltration in psoriatic mice and humans, contributing to psoriatic alopecia.

This study suggests that low-dose IL-2 and IL-15 may help restore immune tolerance in alopecia areata by maintaining Treg cell function, presenting a potential new treatment strategy.

In ex vivo organ culture of human scalp hair follicles, this study found that IL-9 signaling inhibits hair growth, reduces progenitor cell generation, and disrupts immune privilege.

This study found that acne lesions and nonlesional skin in mild-to-moderate acne patients showed significant Th17-skewing and increased antimicrobials, suggesting systemic targets like IL-17/IL-23/IL-36 could be therapeutic.

This study reports that cannabinoid receptor type 1 may influence psoriasis development by modulating laminin-511 expression, suggesting a potential target for treatment.

This study suggests that IL-17 may play a more significant role than IFN-γ in the pathogenesis of chronic alopecia areata, with increasing severity linked to Th17 lymphocytes and cytotoxic T lymphocyte infiltration.

This study found that certain lncRNA gene polymorphisms in HOTAIR and MALAT1 are associated with increased susceptibility to systemic lupus erythematosus, potentially informing clinical applications.

This review discusses genomic and postgenomic alterations in chronic degenerative diseases and potential modulation by dietary and pharmacological agents, reporting no new clinical results.

This study summarizes how the IL-23/IL-17 axis contributes to inflammatory skin diseases like psoriasis and highlights that biologics targeting this pathway, including monoclonal antibodies against IL-23 and IL-17, have shown efficacy in clinical trials for these conditions.

This study found that vimentin is essential for proper wound healing and cell growth by influencing EMT signaling and mTOR activity in mice.

In this study, subcutaneous recombinant human IL-12 showed a 43% partial response rate in early-stage mycosis fungoides patients refractory to previous treatments, with generally mild to moderate adverse events reported.

This study observed that mice treated with mrIL-36α showed differences in wound-induced hair neogenesis compared to those treated with PBS, indicating a potential role of mrIL-36α in hair growth after skin injury.

This study observed that patients receiving IL-2 immunotherapy developed a skin eruption characterized by burning and pruritus, which resolved shortly after stopping the infusion, suggesting that IL-2 mediated these effects.

In a murine model of alopecia areata, this study observed that the IL-2 fusion protein HCW9302 helped prevent disease development by expanding regulatory T cells and reducing disease-causing effector T cell infiltrates, suggesting potential for using IL-2 fusion proteins in alopecia areata treatment.

This study found that innate lymphoid cells-type 1 (ILC1) can induce alopecia areata by disrupting hair follicle immune privilege without the involvement of classical CD8+ T cells.

This study provides evidence that ILC1-like cells can induce alopecia areata in previously healthy human hair follicles, challenging the view that it is solely an autoantigen-dependent autoimmune disease.

This study found that deleting specific super-enhancer regions in mice affects CD25 expression in a cell type-specific manner, leading to autoimmune alopecia in some cases and revealing distinct regulatory mechanisms for constitutive and inducible expression of CD25.

This study investigated dermal fibroblasts in mouse skin using single-cell RNA sequencing and identified signaling pathways that influence adipogenesis, finding that IL-1-NF-κB promotes, while WNT-β-catenin inhibits, the adipogenic potential of these cells, with implications for wound healing and scar formation.

This study found that IL-17 expression was significantly higher in perifollicular fibrosis of active Lichen planopilaris lesions, suggesting that targeting IL-17 could impact the disease's progression.

This study found that topical cepharanthine increased IGF-I production in human dermal papilla cells, suggesting it may stimulate hair growth and be a promising treatment option for androgenetic alopecia.

This research observed that removing RNase L in mice enhances regenerative capacity through increased IL-36 and wound-induced hair neogenesis, highlighting RNase L as a gene that represses regeneration by moderating immune responses during viral infections.

In this study, IL-1α and IL-7 were found to work together to activate epidermal γδ T-cells, which in turn promote hair follicle stem cell proliferation during mouse wound healing.

This systematic review reported an association between specific interleukin gene polymorphisms (IL-17A, IL-18, IL17RA, and IL16) and alopecia areata, suggesting further genetic studies are needed to confirm the interleukins' role in the disorder's progression.

This review discusses the potential of combining low-dose IL-2 with islet antigens to enhance antigen-specific Treg function in type 1 diabetes, but reports no new clinical results.