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This study suggests that human hair follicles may actively suppress natural killer cells, which contrasts with the observed defects in NK cell regulation in alopecia areata.

This review article examines recent studies on the role of diverse immune cells in forming an active niche for hair follicles, offering new insights into hair growth and related diseases.

This study found that immune privilege is preserved in hair follicles of nonsegmental vitiligo patients compared to those with alopecia areata, potentially protecting follicular melanocytes from autoimmune attacks.

This case report describes a rare association where herpes zoster infection may have triggered the first attack of NMOSD with systemic vasculitis in a patient, suggesting potential overlaps in immunopathogenesis.

Corticosteroids and topical irritants are used to treat alopecia areata.

BTNL2 helps protect hair follicles from immune attacks.

This review discusses the pathogenesis and challenges in treating primary cicatricial alopecia, highlighting the need to understand immune protection collapse in hair follicle stem cells; it reports no new clinical results.

This review discusses how modern lifestyle factors affecting gut health may contribute to Alopecia Areata in genetically predisposed individuals, reporting no new results but suggesting the need for long-term interventions.

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.

Intralesional steroids can help regrow hair in some alopecia areata patients but have side effects.

In this study, researchers observed that follicular damage and stem cell loss in frontal fibrosing alopecia may be mediated by immune attacks at the bulge region, suggesting potential for JAK/STAT-targeting treatments to prevent progression.

This review discusses the challenges in identifying specific hair follicle antigens involved in initiating alopecia areata and highlights the need for further research to understand its etiopathogenesis, reporting no new results.

In this review, researchers conclude that immune imbalance between regulatory and cytotoxic T cells, along with activation of IFN-γ–MHC and IL-15–NK pathways, disrupts hair follicle immune privilege, suggesting pivotal mechanisms in alopecia areata development and potential targets for immunotherapeutic interventions.

TGF-β is found in hair follicles and may cause hair loss in alopecia areata.

This review highlights that alopecia areata is influenced by genetic, autoimmune, and environmental factors, with emerging treatments like JAK-2 inhibitors showing promise for severe cases.

In this study, researchers found that in mice, gonadal hormones and biological sex do not affect the expression of SARS-CoV-2 entry proteins ACE-2 and TMPRSS-2 in the respiratory tract, regardless of disease state.

This review discusses recent advances in the treatment of alopecia areata, highlighting new potential therapies like JAK inhibitors and PRP, and reports no new clinical results.

This study observed a rare case of alopecia areata with granulomatous inflammation, successfully treated with intralesional triamcinolone, leading to complete hair regrowth within two months, highlighting the need for careful diagnosis to distinguish it from other granulomatous alopecias.

This study describes alopecia areata as a long-term, immune-mediated disorder characterized by non-scarring hair loss, often occurring in genetically predisposed individuals and possibly triggered by T-cell-mediated inflammation, environmental stressors, and genetic factors.

This study explains that alopecia areata, a long-term immune-mediated disorder causing patchy baldness, results from an immunological attack on hair follicles, often in genetically predisposed individuals, with a complex mix of immunological, environmental, and genetic factors involved in its development.

This source explores alopecia areata, an immune-mediated disorder causing patchy hair loss due to immunological attacks on hair follicles, with a complex interaction of genetic, environmental, and immunological factors, particularly T-cell-mediated inflammation, contributing to its onset.

In this research, the authors describe alopecia areata as a long-term, immune-mediated disorder that causes non-scarring hair loss due to an immunological attack on hair follicles, often occurring in genetically predisposed individuals and manifesting in childhood or early adulthood.

This abstract explains that alopecia areata is an immune-mediated condition causing non-scarring hair loss, typically in genetically predisposed individuals, with its etiology linked to immune dysregulation, environmental stressors, and genetic factors.

This source describes alopecia areata as a long-term, immune-mediated disorder causing non-scarring hair loss, often starting in childhood or early adulthood due to genetic predisposition and an immunological attack on hair follicles.

Certain CD8+ T cells attack hair follicles in alopecia areata, suggesting they could be targeted for treatment.

This study reported that CXCL12 may have a dual role in alopecia areata, where decreased levels could impair angiogenesis and disrupt vascular support to hair follicles, while its overexpression might exacerbate autoimmune attacks on hair follicles, contributing to hair loss.

This research explored the pathogenesis of alopecia areata, finding that disrupted immune tolerance and gut microbiota are significant contributors, and highlighted the need for innovative treatments that restore immune tolerance and modulate gut microbiota to improve patient outcomes.

In this study, a mouse model of scarring alopecia demonstrated significantly reduced CD200R expression in affected skin, which may contribute to immune attacks on hair follicles.

Trichohyalin in hair can trigger immune attacks in alopecia areata.

This study found that in mice, perforin-mediated cytolysis by CD8 T cells is not necessary for the autoimmune attack on hair follicles in alopecia areata, suggesting other mechanisms are responsible for disease progression.