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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 review discusses the potential of JAK inhibitors as a promising treatment strategy for alopecia areata, highlighting their mechanism and recent FDA approval based on clinical trial efficacy.

This study found that the OVOL1 gene in mouse neonatal dermal cells is crucial for hair follicle neogenesis, suggesting it plays a significant role in maintaining trichogenicity.

This study found that the cytokine-mediated signaling pathway is the primary pathway disrupted in skin after CO2 laser surgery.

This study demonstrated the expression of type 1 interferon-related proteins in inflammatory lesions of alopecia areata, showing a distinct distribution pattern compared to cicatricial alopecia.

In this study, researchers found that changes in immune cell infiltration and immune-related gene expression may contribute to the immune microenvironment changes in male androgenetic alopecia.

This study observed distinct plasma miRNA profiles in alopecia areata, identifying several miRNAs downregulated in both mild and severe forms; machine learning models demonstrated strong predictive accuracy, and kinase inhibitors were suggested as promising therapeutic targets based on pathway analysis.

This study found that certain T cell-associated genes were upregulated in dogs with Vogt-Koyanagi-Harada syndrome and vitiligo, suggesting a shared immunopathogenesis with humans.

This study found that Enz_MoriL, a compound derived from Morus alba L., promotes hair follicle cell proliferation by affecting the Wnt/β-catenin pathway and can counteract an alopecia areata-like condition by suppressing the JAK-STAT signaling in human hair follicle dermal papilla cells.

This study identified a novel G207E STING mutation associated with severe inflammatory symptoms and suggested that common polymorphisms in TMEM173 and IFIH1 may modify the phenotype in affected individuals.

This study reports that a novel gain-of-function mutation in TMEM173, combined with polymorphisms in TMEM173 and IFIH1, results in a distinct clinical phenotype with features of SAVI, including alopecia and photosensitivity.

Discoid lupus erythematosus involves immune activation and fibrosis around hair follicles, with shared pathways across humans, dogs, and mice, suggesting potential treatments for both humans and animals.

This study explored COVID-related chilblains using transcriptomics and found they showed a distinct interferon and JAK/STAT pathway activation, absent in vaccine-related chilblains, with inflammatory cell types varying over time.

This study found that specific gene upregulations and mutations in hidradenitis suppurativa skin support the role of inflammation, altered epithelial differentiation, and metabolism dysregulation in the disease's pathogenesis.

This chapter reviews recent developments in vitiligo research, highlighting the role of melanocyte stem cell differentiation and oxidative stress in its management, but reports no new clinical results.

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 systematically reviewed literature on paradoxical reactions during biologic treatments for psoriasis, identifying immune dysregulation mechanisms and diverse clinical manifestations, highlighting that mild cases often respond well to topical treatments, while severe cases may require switching to different IL-23 inhibitors.

This study conducted a scoping review and meta-analysis revealing a complex chemokine profile in alopecia areata patients, with elevated Th1, Th2, and other immune pathway chemokines, suggesting broader immunomodulatory strategies may help address the disease's multifaceted immune dysregulation.

In this scoping review and meta-analysis, researchers found that patients with alopecia areata show a complex serum chemokine profile, predominantly involving Th1- and Th2-associated chemokines, suggesting that broader immunomodulatory strategies might address the diverse immune dysregulation observed in the disease.

This study found that hair follicle stem cells from hidradenitis suppurativa patients showed alterations in cell cycle regulation and DNA replication, potentially linking genetic predisposition to the skin inflammation characteristic of the disease.

This review discusses current and emerging treatments for discoid lupus erythematosus, suggesting that new biologic and small-molecule therapies may improve disease control when combined with traditional management.

This case report discusses a successful treatment of Alopecia Areata with tofacitinib and includes a literature review on the condition's pathophysiology and the mechanism of JAK inhibitors, though it notes the high failure rate of available treatments and absence of FDA-approved options.

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 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 review examines the pathophysiological mechanisms and emerging targeted treatments for alopecia areata, particularly highlighting the efficacy of oral JAK inhibitors over other less effective alternatives.

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.

This study found that type I interferon response-related genes activated by RIG-1 and IL-17 pathways were significantly up-regulated in hair follicle and skin samples with chronic discoidal lupus erythematosus.

In this study, Wang et al. (2022) found that in patients with cutaneous lupus erythematosus, chronic lesions contained more senescent progenitor cells, marked by p16 and p21, than subacute lesions, suggesting a link between disease chronicity and cellular senescence.

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.

This study found that impairments in cholesterol biosynthesis in hair follicles of primary cicatricial alopecia patients trigger an inflammatory immune response, potentially linking sterols to inflammation in the disease's pathogenesis.