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This review discusses the mechanisms underlying the collapse of hair follicle immune privilege in alopecia areata and emphasizes the importance of therapeutic strategies aimed at restoring immune tolerance.

In this study, single-cell sequencing revealed clonal expansions of CD4+ and CD8+ T cells in murine and human alopecia areata, supporting the development of predictive models for human disease.

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.

The study investigated immune cell patterns around the hair follicle infundibulum in androgenetic alopecia, revealing significant differences in immune signatures between patients with AGA and control donors, specifically noting an enrichment of CD4 cells in the patient group.

This study identified key genetic regions associated with alopecia areata, highlighting both acquired and innate immune involvement, with a novel link to the upregulation of ULBP ligands in autoimmune disease.

This study found that combining hair transplantation with platelet-rich plasma treatment significantly improved hair regeneration, reduced hair loss, and minimized skin lesion areas in patients with androgenic alopecia compared to hair transplantation alone, suggesting enhanced treatment efficacy.

This study found that terminally differentiated effector memory Vδ1T-cells and their cytotoxic activation markers were elevated in alopecia areata patients, suggesting these cells may contribute to its early pathogenesis.

This study suggests that hypersensitivity and increased serum IgE levels might contribute to the pathogenesis of diffuse alopecia areata through intense local inflammatory infiltration.

This study describes a new mouse model for vitiligo that mimics key clinical features such as skin depigmentation and CD8 + T cell infiltration, providing a useful tool for in-depth research and drug discovery.

In this study, researchers observed elevated levels of epidermal γδ T cells, keratinocytes, and an upregulation of the BST2 gene among immune cells in C3H/HeJ mice with alopecia areata, suggesting a potential role in disease pathogenesis.

In this study, the researchers found that treatment with the JAK inhibitor tofacitinib in alopecia areata patients may reduce clonal CD8+ T cell expansions but does not eliminate them entirely, which could contribute to disease relapse.

This study found that in alopecia areata, treatment with the oral JAK-inhibitor tofacitinib decreased clonally expanded CD8⁺ T cells in the scalp, but many expanded clones did not completely disappear, potentially leading to relapse after stopping treatment.

In this narrative review, researchers outlined the role of T cells in the autoimmune pathogenesis of alopecia areata and highlighted ongoing research into therapeutic pathways, beyond current JAK inhibitors, aimed at developing new treatments for the disease.

In this study, blocking the CXCR3 receptor in mice prevented the development of alopecia areata by inhibiting the accumulation of specific T cells in the skin, suggesting a potential therapeutic approach for humans.

This study found that antroquinonol inhibited CD8+ T cell proliferation and reduced proinflammatory cytokine secretion in vitro, while also ameliorating H2O2-induced depigmentation and resisting reductions in hair follicle length, skin thickness, and tyrosinase expression in mice.

This paper proposes that the induction of HF-specific neo-antigens by peripheral CD8+ T cells may maintain self-tolerance but could also lead to immunopathology in conditions like alopecia areata.

In this study, researchers found that CD4 T cells from the skin draining lymph nodes of mice with alopecia areata can transfer the disease to recipient mice, highlighting the key role of these cells and their interaction with CD8 T cells in the disease's development.

This review discusses the bidirectional interactions between human mast cells and CD8 T cells in the skin, particularly in the context of disorders like psoriasis, atopic dermatitis, and vitiligo, and reports no new findings.

This study found that NK and CD8+ T cell infiltration may drive inflammation in androgenetic alopecia, suggesting that targeting IL-15 signaling could offer a new therapeutic approach for hair regeneration.

This study suggests that SOCS3 treatment may effectively inhibit alopecia areata by suppressing CD8+ T cell activity and IFN-γ production.

This review discusses the potential of targeting Coenzyme A metabolism to restore metabolic balance, reduce chronic inflammation, and enhance immune function, particularly by modulating Vitamin B5 pathways involved in Th17-mediated inflammation and CD8-dependent anti-tumor immunity.

This study found that Ifidancitinib, a JAK1/3 inhibitor, significantly promoted hair regrowth and reduced inflammation in a mouse model of alopecia areata by decreasing pathogenic T cell activity and inducing T cell exhaustion.

This review discusses how tissue resident memory T cells contribute to autoimmune skin diseases like vitiligo and psoriasis, highlighting their role in continuous immune activation, and reports no new clinical results.

Resident memory T cells and necroptosis may drive fibrosis in eosinophilic fasciitis and morphea.

This study found that in chronic alopecia areata, increased IL-17 expression and CD8+CD49a-Trm cell infiltration in hair follicles were associated with more severe histopathologic gradings, while Foxp3+mTreg infiltration decreased.

This review explores the role of Tregs in autoimmune skin diseases, transplantation, and skin cancer, and discusses Tregs-based therapies' potential for treating autoimmunity without reporting new experimental results.

The study suggests that refractory chronic alopecia areata cases have more infiltrating skin resident memory T cells, and using a JAK inhibitor may be an effective treatment option.

The authors concluded that increasing regulatory T cells in patients with alopecia areata may improve hair follicle regeneration by reducing autoimmune responses, suggesting a potential new therapeutic approach since current treatments are often ineffective with high relapse rates.

In this study, researchers demonstrated that CD4 T cells from skin-draining lymph nodes in mice with alopecia areata can transfer the disease to recipient mice, revealing a critical role for CD4 T cells in disease development and suggesting potential therapeutic targets.

In this study, iNKT10 cells were found to play a significant role in preventing and treating alopecia areata in a humanized mouse model, suggesting these cells could have potential in managing related autoimmune disorders.