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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.

In this study, nearly 5% of anti-TNF-treated patients with IBD developed psoriasiform skin lesions, with smoking identified as a main risk factor, and ustekinumab proved highly effective in severe cases.

Targeting MIG and MCP-1 may help treat inflammation in alopecia areata.

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 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 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.

Lasheras-Pérez et al. reported that JAK3 and TYK2 proteins are activated in certain forms of primary cicatricial alopecia, suggesting the JAK/TYK/STAT pathway as a potential therapeutic target for these conditions.

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 identified specific genes upregulated in skin γδ T cells involved in alopecia areata, with findings suggesting these cells contribute to disease pathogenesis through inflammatory and Th1 response mechanisms in mouse and possibly human skin.

This study found that activating Wnt/beta-catenin signaling in hair follicles is sufficient to induce adipocyte generation in the dermis, affecting both hair follicle stem cell activation and adipocyte differentiation.

This study observed that both ritlecitinib and brepocitinib improved scalp biomarkers in patients with alopecia areata, with associations to hair regrowth seen in this phase 2a trial.

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.

In this study, researchers classified melanomas by filaggrin expression levels and found that in filaggrin^High melanomas, there are significant changes in FGFR signaling and impaired GNA14 and Th1 signatures, linked to genetic and immune alterations associated with pruritus.

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.

This research found that reduced expression of SIRT1 in human scalp tissue may contribute to alopecia areata development by inducing immune-inflammatory responses in hair follicle cells, suggesting that SIRT1 plays a regulatory role in hair follicle immunity.

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.

This study identified shared gene expression changes and immune cell infiltration patterns that may contribute to hair loss in alopecia areata and cutaneous lupus erythematosus, but also highlighted factors that might preserve hair in psoriasis patients.

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 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, increased production of CXCL10 was associated with the infiltration of Th1 and Tc1 cells in acute alopecia areata, suggesting a possible new target for treatment.

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 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.

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 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 observed that Epigallocatechin-3-gallate (EGCG) can inhibit phosphorylation of STAT1 and reduce a specific subset of immune cells in vitro and ex vivo, suggesting a potential role in maintaining immune privilege in alopecia areata.

This study found that immune privilege collapse in the hair follicle bulge and associated immune responses may contribute significantly to the pathogenesis of lichen planopilaris, suggesting a potential autoimmune basis for the disease.