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This study found that patients with active severe alopecia areata exhibited decreased CD200 expression on T and B lymphocytes, which may be linked to an imbalance in Th1/Th2 immune equilibrium.

This study conducted a meta-analysis of gene expression data from alopecia areata patients, identifying 5109 differentially expressed genes and highlighting enriched pathways like JAK-STAT signaling, providing insights into the disease's pathogenesis and potential treatment targets.

This study found that canine pemphigus foliaceus skin lesions exhibit a distinct immune signature, with upregulated pro-inflammatory and Th17-related genes, showing similarities to human pemphigus. Further research using advanced sequencing is needed to better understand the disease's pathogenesis.

This study found that both Th1 and Th2 cytokine markers were elevated in the serum and skin of patients with alopecia areata, with Th2 markers more closely linked to disease severity.

This study found that intracellular Toll-like receptors were significantly up-regulated in peripheral blood mononuclear cells of alopecia areata patients, suggesting a potential role in inflammatory signaling and pathogenesis.

This study found that reduced expression of CD200R1 on monocyte-derived macrophages in rheumatoid arthritis patients was significantly associated with higher disease severity and an imbalance in Th17/Treg cells.

This study observed significant differences in immune cell infiltration and gene expression across different skin sites, with the back displaying higher tolerance-promoting immune mechanisms, which may enhance epicutaneous immunotherapy outcomes.

Alopecia totalis/universalis involves more intense immune activity and inflammation than patchy alopecia areata.

This study found that both Th1 and Th2 immune responses, along with IL-23 and IL-32 cytokine pathways, are active in alopecia areata lesions, and corticosteroid injections significantly altered these immune markers.

This study found that EGFR-targeted cancer therapy can cause skin toxicities by disrupting epidermal signaling, allowing microbiota invasion and inflammation, but identified a potential treatment approach using FGF7 or SOS expression to restore barrier integrity.

This study found that a quinazoline derivative, SH-340, increased skin barrier-associated factors and inhibited TSLP expression and STAT6 phosphorylation in human primary keratinocytes, suggesting potential benefits for alleviating inflammation and improving skin barrier function in atopic dermatitis.

This study reviewed the expression of chemokines in patients with alopecia areata, finding elevated Th1 and Th2 chemokine levels, suggesting a complex immune profile that may require broad immunomodulatory strategies to address the disease's underlying immune dysregulation.

In this study, researchers found that using a 5-α reductase inhibitor may reduce inflammation-related cytokines associated with T-helper cell 1 and T-helper cell 2 in prostate tissues after surgery, but it did not affect those related to Th17 cells.

This study observed an association between intense itching in anterior chest keloids and an increased density of nerve fibers in the epidermis, alongside elevated expression of the pruritus mediator substance P, though no difference was found in Langerhans cells related to pruritus, location, or region.

In this study, researchers observed that intractable pruritus in anterior chest keloid lesions is linked to increased intraepidermal nerve fibre density and elevated expression of substance P, without differences in Langerhans cells across different keloid regions.

This study found that oral JAK3 and TYK2/JAK1 inhibitors improved clinical outcomes in alopecia areata patients by reducing immune responses and enhancing hair keratin expression, with stronger effects in those with shorter disease duration.

In this study, researchers developed a mouse model of scarring alopecia and observed significant reductions in CD200R expression in affected skin, potentially linking this signaling pathway to immune attacks on hair follicles and suggesting new treatment targets for scarring hair loss.

In this study, researchers reported that the Pinkie mutation in mice, affecting RXRa activity, leads to skewed Th1 development and suggests RXRa's role in Th2 differentiation, impacting immune responses.

Targeting immune pathways like JAK/STAT may help treat frontal fibrosing alopecia.

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 carbonic anhydrase II was significantly upregulated in human keratinocytes when treated with toll-like receptor 3 agonist and Th2 cytokines, suggesting its potential role in inflammatory skin conditions.

The study investigated immune cell patterns around the hair follicle infundibulum in androgenetic alopecia, revealing significant differences in immune signatures between patients with AGA and control donors, specifically noting an enrichment of CD4 cells in the patient group.

This study found that local injections of interleukin-4 and neutralizing anti-interferon-γ antibody effectively treated alopecia in a mouse model, suggesting potential therapeutic pathways for human alopecia areata.

This study found that selective deletion of Ctip2 in epidermal keratinocytes in adult mice leads to atopic dermatitis-like inflammation and suggests Ctip2 plays a crucial role in skin barrier maintenance and inflammatory regulation.

In this study, topical naringin was found to significantly improve dermatitis severity and reduce inflammatory markers in a mouse model of atopic dermatitis, suggesting its potential as a therapeutic agent for this condition.

In this study, researchers found that cytokine dysregulation linked to genetic background is present in both patients and healthy but genetically related individuals in two autoimmune skin diseases, Pemphigus vulgaris and Alopecia areata, suggesting that protective immune mechanisms may prevent disease manifestation in predisposed individuals.

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 found that acne lesions and nonlesional skin in mild-to-moderate acne patients showed significant Th17-skewing and increased antimicrobials, suggesting systemic targets like IL-17/IL-23/IL-36 could be therapeutic.

This study identified a distinct cytokine activation signature in alopecia areata, involving TH2, TH1, IL-23, and IL-9/TH9 pathways, suggesting potential targeting strategies similar to those in psoriasis and atopic dermatitis.

This study found that osteopontin expression was significantly higher in alopecia areata lesions compared to healthy controls, suggesting it may play a role in the disease's pathogenesis.