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Postmenopausal women may experience frontal hairline and eyebrow loss due to cicatricial fibrosis.

This study identified a reduced frequency of IL-10-producing regulatory B cells in alopecia areata patients, suggesting a protective role by these cells in disease development by regulating key immune mediators, such as IFN-γ and NKG2D+CD8+ T cells.

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.

Contact immunotherapy can change immune responses in alopecia areata, suggesting new treatment targets.

This study found that selectively targeting HDAC4 and HDAC7 in mice can reduce Th17 cell-mediated intestinal inflammation, suggesting a potential treatment approach for Th17-related inflammatory diseases like ulcerative colitis.

In this case report, mogamulizumab treatment for Sézary syndrome was associated with rashes and alopecia in a patient, highlighting the potential for immune-mediated side effects and suggesting that such adverse effects might indicate a favorable prognosis, though further studies are needed.

This review summarizes recent findings about the multi-site differentiation of tissue regulatory T cells, emphasizing the pivotal role of epigenetic remodeling, but it reports no new clinical results.

This study provides a detailed analysis of cell subpopulations in a mouse model of wound-induced hair follicle regeneration, revealing specific cellular dynamics and heterogeneity that may influence hair follicle neogenesis.

This manuscript reviews the latest understanding of alopecia areata's pathogenesis, highlighting the roles of genetic, immunological, and environmental factors, with a focus on immune responses involving IFN-γ and cytotoxic CD8+ T-cells as key contributors to hair follicle inflammation and function disruption without follicle destruction.

Alopecia areata patients have more activated T cells in their blood, which may help in developing treatments.

This study found that alopecia areata is linked to genetic factors, specifically HLA haplotypes on chromosome 6, and involves immune privilege collapse at hair follicles which is mediated by the JAK-STAT pathway and pro-inflammatory cytokines like IFN-γ.

In this case study, a 65-year-old male with hepatocellular carcinoma treated with the PD-1 inhibitor Sintilimab developed alopecia universalis alongside significant tumor regression and complete remission, highlighting a rare immune-related adverse event with effective anti-tumor outcomes.

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.

This review discusses immune privilege in anagen hair follicles and its collapse in alopecia areata, emphasizing the importance of restoring this function for effective management and disease relapse prevention.

This study found that JAK inhibitors promote hair regrowth in both mice and human alopecia areata cases by blocking key immune pathways involved in disease development.

This study found that patients with RASopathies have lower serum IgA and CD8 levels compared to controls, indicating a potential risk for developing autoimmune disorders.

T cells affect skin cell genes in inflammatory diseases, and therapy can normalize these changes.

This study found that injecting mouse hair follicle-derived mesenchymal stem cells (moMSCORS) into C57BL/6 mice reduced the incidence and severity of type 1 diabetes by modulating immune responses, suggesting potential for therapeutic use due to their immunosuppressive effects.

This study found that CD80 expression in wound-activated hair follicle stem cells induces Foxp3 expression in effector T cells, facilitating wound repair by converting them into regulatory T cells.

This study found that overexpression of miR-1246 in peripheral CD4+ T cells can reduce markers associated with inflammation and T cell activation in severe active alopecia areata, suggesting potential therapeutic benefits.

This review discusses emerging research areas in alopecia areata pathobiology, highlighting the potential roles of unconventional immune cells and the need for more targeted therapeutic strategies, but reports no new experimental results.

In this study, selective inhibition of JAK3 signaling effectively prevented and reversed alopecia areata in a mouse model, while JAK2 inhibitors did not restore hair growth.

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 mathematical model of alopecia areata illustrates how inflammatory autoimmune responses interrupt the anagen phase of hair growth, and may help evaluate treatments and identify new therapeutic targets.

Harris et al. describe a new mouse model for vitiligo, where interfollicular melanocytes are retained and melanocyte-targeting immune responses are simulated, aiding the development of immunomodulatory therapies.

This study examines the similarities and differences in the pathogenesis of autoimmune conditions alopecia areata and vitiligo, highlighting shared features like immune cell involvement and cytokine pathways, while noting differing immune responses in skin and hair.

This review discusses the mechanisms behind alopecia areata and primary cicatricial alopecia and reports no new clinical results, aiming to guide the development of targeted treatments.

This review summarizes the pathophysiology and immune mechanisms of inflammatory skin diseases like psoriasis and atopic dermatitis, highlighting the therapeutic potential of targeted immunotherapies, but reports no new clinical results.

This article proposes that alopecia areata may be caused by immune attacks on hair follicles after an immune privilege collapse, suggesting new therapeutic approaches targeting this immune response pattern.