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This study found that patients with alopecia areata and their healthy family members had elevated levels of Th1- and Th17-related cytokines, suggesting a genetic link in cytokine dysregulation.

This study found that forming inclusion complexes of DPCP with HPβCD using the 3D ground mixture method enhances its anti-inflammatory activity at lower doses compared to complexes with β-CD.

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, researchers developed a novel topical gel combining minoxidil and JAK inhibitor tofacitinib, which effectively enhanced hair follicle growth and reduced local inflammation in mice with alopecia areata, suggesting a new approach for treating this condition.

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 pro-inflammatory cytokines and apoptotic mechanisms, specifically involving granzyme B and Fas pathways, are associated with chronic alopecia areata, indicating their potential role in the disease's persistence.

This review identifies shared interferon gamma-driven immune pathways in vitiligo and alopecia areata, revealing potential targets for new treatments, but reports no clinical results.

This study suggests that αMSH may play a regulatory role in human dermal papilla cells, potentially influencing immune and inflammatory responses in hair follicles, which could contribute to inflammatory alopecia.

Alopecia areata severity is linked to increased TH1 and TH2 activity.

This study found that azathioprine may improve relapses and disability in patients with neuromyelitis optica spectrum disorder but is associated with higher adverse events compared to mycophenolate mofetil.

This study highlights the need for further research on dysregulated immune and fibrotic pathways in morphea to better understand its pathogenesis and develop new biomarkers and therapies.

This article discusses the potential of oral tofacitinib as a treatment for atopic dermatitis, alopecia areata, and vitiligo, without presenting new clinical results.

This study demonstrates that T-cell responses in extensive alopecia areata scalp may be aberrantly regulated, with reduced cytokine production but activated phenotype, providing insight into the disease's immune mechanisms.

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 found that anthralin and mechlorethamine were the most effective therapies among those tested in AA-affected rodent models, providing a basis for further analysis of their mechanisms in Alopecia Areata.

This study found that ruxolitinib modulated inflammatory changes and stimulated growth factor signals by blocking the JAK-STAT pathway in an in vitro model of alopecia areata.

This study suggests that mesenchymal stem cell therapy may improve cell viability and regulate key signaling pathways in vitro for treating alopecia areata.

This study found that human hematopoietic mesenchymal stem cells increased the viability and migration of human outer root sheath cells in an in vitro alopecia areata model, involving Wnt/β-catenin and JAK/STAT pathways.

This case report describes a patient with Crohn's disease developing alopecia and psoriasiform skin lesions while on adalimumab treatment.

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 patients with alopecia areata had a significant increase in NKG2D+CD4+ T cell levels in their blood compared to healthy controls.

This study reports a notable case of a patient with psoriatic arthritis and alopecia universalis who experienced significant improvement in both conditions after treatment with the JAK1 selective inhibitor upadacitinib, suggesting its potential efficacy for alopecia universalis, especially in cases involving inflammatory arthritis.

This review discusses the complex role of immune disturbances and the JAK-STAT pathway in alopecia areata, noting the success of JAK inhibitors in treatment, while highlighting ongoing debates and challenges in targeting other pathways like IL-17 and TNF-α.

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 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.

This study observed that individuals with Down syndrome exhibit early immune dysregulation, including multi-organ autoimmunity and hypercytokinemia, and found that the JAK inhibitor tofacitinib showed a good safety profile and reduced skin pathology in a Phase II trial.

This review discusses the current understanding of frontal fibrosing alopecia's pathogenesis, highlighting genetic susceptibility, immune response involvement, and possible links to steroid hormones, but reports no new clinical results.

This study suggests that frontal fibrosing alopecia is a highly inflammatory disease involving TH1 and JAK-STAT pathways, without reduced hair keratins, highlighting JAK-STAT signaling as a potential therapeutic target.

Specific immune cells cause alopecia areata and blocking certain proteins can prevent it.

A JAK1 variant causes hair loss, skin issues, and thyroid disease, but treatment with a specific inhibitor can help.