November 2025 in “Frontiers in Immunology” This review discusses the role of immune cells in the pathogenesis of alopecia areata and highlights emerging immunomodulatory strategies and novel therapeutic targets aimed at offering more effective and durable treatments for this autoimmune hair loss disorder.
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.
April 2021 in “Sohag Medical Journal” This review outlines the proposed theories behind the development of alopecia areata, emphasizing the autoimmune process involving lost immune privilege in hair follicles, and stresses the need to pinpoint specific pathogenic mechanisms for potential treatments.
April 2019 in “Journal of Investigative Dermatology” Gut microbiota influences the development of alopecia areata.
February 2018 in “Trends in Immunology” This study demonstrated that antigens from the skin bacterium Staphylococcus epidermidis can stimulate CD8+ T cells, which in turn enhance wound healing.
162 citations
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October 2014 in “Autoimmunity reviews” This review discusses alopecia areata, highlighting its autoimmune aspects, environmental triggers, and current treatment options, but reports no new clinical results; recent studies suggest JAK pathway intervention may offer therapeutic potential.
57 citations
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April 2019 in “British journal of dermatology/British journal of dermatology, Supplement” This background review discusses alopecia areata, highlighting the role of CD8+NKG2D+ T cells in hair follicle pathogenesis, and notes that the exact mechanisms causing hair loss remain unclear.
26 citations
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September 2013 in “Journal of Dermatological Science” In this study, researchers found that serum granulysin levels might serve as a novel marker for disease activity in acute alopecia areata, being significantly associated with broader bald skin areas, poorer prognosis, and co-existing allergic disorders.
23 citations
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April 2021 in “Journal of Clinical Medicine” This review compiles existing data on frontal fibrosing alopecia and highlights the promise of 5-alpha reductase inhibitors as a treatment option, while noting the need for clarity on its cause and progression.
15 citations
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January 2022 in “Immune Network/Immune network” 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.
13 citations
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August 2017 in “Journal of Cellular Physiology” In this study, researchers found that in mouse models of alopecia areata, the expression of immune-regulating molecules PD-L1 and PD-L2 in dermal fibroblasts is increased by activated T cells, potentially indicating a lack of negative immune control in affected skin.
12 citations
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September 2022 in “Frontiers in Genetics” This study identified seven genes that may serve as biomarkers for diagnosing skin cutaneous melanoma by analyzing the relationship between UV exposure, ferroptosis, and the cancer's pathology.
11 citations
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October 2021 in “Orphanet journal of rare diseases” 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.
10 citations
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September 2014 in “European Journal of Dermatology” This case report describes a 29-year-old woman with longstanding alopecia areata who experienced improvement in her scalp hair loss after 7 years of topical treatment with squaric acid dibutylester.
9 citations
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February 2022 in “Nature communications” This study identified KRT82 as a significant Alopecia Areata risk gene, finding that rare damaging variants are linked to elevated immune cell infiltration around hair follicles in affected individuals.
4 citations
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April 2024 in “Journal of Drugs in Dermatology” In this case report, a severe case of pediatric alopecia areata was treated with topical ruxolitinib, a Janus kinase inhibitor, highlighting the limited but promising evidence for this treatment in children.
2 citations
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May 2023 in “The Journal of Immunology” This animal study observed that treatment with the S1PR modulator NXC736 significantly reduced lesion area and CD8+ T cell infiltration in mice with alopecia areata, suggesting its potential as a promising therapy for the condition.
2 citations
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January 2020 in “Enlighten: Theses (The University of Glasgow)” This study found that alopecia areata is associated with distinct systemic and tissue immune signatures, with macrophages implicated as contributors to hair loss, suggesting potential therapeutic targeting of macrophage activity.
2 citations
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September 2014 in “Nature reviews. Drug discover/Nature reviews. Drug discovery” Specific immune cells cause alopecia areata and blocking certain proteins can prevent it.
1 citations
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September 2023 in “JAAD case reports” 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.
1 citations
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September 2013 in “The Journal of Dermatology” An 8-year-old girl developed a rare skin condition in a linear pattern on one side of her body after a lung infection, which improved with treatment.
This study developed a silk fibroin/poly(vinyl alcohol) microneedle loaded with α-aminoxyacetate and HfO2 nanoparticles for vitiligo treatment, which protected against ROS damage and modulated immune responses, leading to improved melanogenesis and skin repigmentation.
June 2026 in “Zenodo (CERN European Organization for Nuclear Research)” This review compiles current insights into alopecia areata's epidemiology, immune mechanisms, diagnosis, treatment options, including novel JAK inhibitors, and its severe psychosocial impact, while also highlighting emerging research areas.
June 2026 in “Zenodo (CERN European Organization for Nuclear Research)” This source reviews alopecia areata, highlighting its epidemiology, immune-related causes, diagnostic methods, and the shift in treatment with JAK inhibitors like baricitinib and ritlecitinib, marking the first disease-modifying options for this hair loss condition.
January 2026 in “Forum Dermatologicum” This review examines various pharmacological options for managing alopecia areata, highlighting the effectiveness of corticosteroids for mild to moderate cases and promising results from JAK inhibitors like baricitinib for more severe forms, with additional benefits from minoxidil and potential from other treatments.
This review discusses the approval of deuruxolitinib, an oral JAK inhibitor, by the FDA in July 2024 for treating severe alopecia areata in adults, highlighting its role as the third approved oral treatment option alongside baricitinib and ritlecitinib.
November 2025 in “The Journal of Immunology” This study observed that in human scalp hair follicles, BTNL2 expression is lower in stressed conditions, which correlates with increased cytotoxic activity by gamma/delta and CD8+ T cells, suggesting a possible role for BTNL2 in controlling immune responses relevant to alopecia areata.
November 2025 in “The Journal of Immunology” This study found that administering an S1PR 1&4 modulator reduced alopecia areata lesion size and decreased CD8+ T cell infiltration in mice, suggesting potential as a treatment for this condition.
This article hypothesizes that thymoma with aplastic anemia may result from abnormal autoimmune CD8+ T lymphocytes produced by the thymoma, potentially leading to other cytotoxic T-cell-mediated autoimmune diseases.
May 2025 in “Frontiers in Pharmacology” This study investigated alopecia areata in a mouse model, finding that tofacitinib may inhibit disease progression by modulating linoleic acid metabolism and magnesium pathways, particularly affecting CD8+ T cell infiltration in hair follicles, offering insights for potential treatments.