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This study found that treatment with EGFR inhibitors or mitogen-activated kinase inhibitors may compromise the immune privilege of human scalp hair follicles, suggesting new directions for managing drug-induced folliculitis.

This review discusses the multifaceted roles of regulatory T cells in cutaneous wound healing and highlights potential therapeutic strategies targeting these cells to enhance wound repair in chronic and diabetic wounds, but reports no new clinical results.

In this study, researchers created a detailed human skin cell atlas by analyzing over 700,000 cells, finding that disrupted communication among specific immune and stromal cell subsets may play a key role in initiating and sustaining chronic skin inflammation in atopic dermatitis.

In this study, Treg depletion impaired skin wound healing in mice, potentially by altering the cytokine environment and expanding certain T-cell populations, disrupting the normal healing process.

This study found that pro-inflammatory cytokines and apoptotic mechanisms, specifically involving granzyme B and Fas pathways, are associated with chronic alopecia areata, indicating their potential role in the disease's persistence.

This study found that Schistosoma mansoni cercariae stimulate epidermal keratinocytes in mice, initiating pro-inflammatory responses and barrier repair mechanisms akin to those in wound healing.

This study suggests that allogenic human mesenchymal stem cell treatments have potential therapeutic effects by inducing immune tolerance and anti-inflammatory effects in severe alopecia areata patients.

In a mouse model, this study found that exposure to PM2.5 leads to significant postpartum hair loss, apparent via morphological changes and elevated markers of inflammation, apoptosis, and fibrosis, potentially exacerbated by changes in hormone receptors and stem cell populations.

This review highlights how chronic inflammatory skin disorders like psoriasis and atopic dermatitis may be better understood as manifestations of systemic immune dysregulation rather than just skin issues, suggesting that recognizing these conditions as markers of broader immune imbalance can improve diagnosis and medical education.

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.

This article discusses inflammatory perifollicular fibrosis and alopecia but provides no new research findings.

This study reports that two mouse models of scarring alopecia exhibit similar patterns of hair loss progression despite histological differences in inflammatory cell localization and MHC class I expression.

This study discusses the epithelial-immune microenvironment in chronic skin diseases, such as psoriasis and atopic dermatitis, and highlights current and future treatment strategies targeting inflammatory loops within these diseases.

This study found that TNC + fibroblasts are crucial in neuro-immune interactions in various skin diseases, particularly inflammation and tumors, by engaging extensively with immune cells and overexpressing inflammatory genes, suggesting their significant role in skin abnormalities.

This study found that Imaging Mass Cytometry effectively visualizes multiple biomarkers in alopecia areata, enhancing analysis of immune cell and tissue interactions in hair pathology.

This study found that CD1a-restricted CD4+ T cells responsive to lysyl-phosphatidylglycerol were more frequent in the blood of atopic dermatitis patients, suggesting a potential role in the disease's Th2-mediated pathology.

In this study, Alox15 knockout mice exhibited disrupted skin integrity and increased inflammation, suggesting that Alox15-mediated resolvin D2 production is crucial for maintaining skin homeostasis by suppressing inflammation.

This study found that UV-B exposure significantly increased the expression of inflammatory cytokines IL-1β and IL-8 in cultured sebocytes.

This study found that specific inflammatory factors, including decreased SCF, MIP-1β, and MCP-1, and increased SDF-1α and HGF, have causal relationships with rosacea, highlighting potential targets for further research into disease mechanisms.

This thesis presents a new scientific approach using specific models to gain insights into psoriasis and eczema, highlighting a molecular classifier that improves diagnostic accuracy and predicts therapeutic response for these conditions.

This study concluded that myositis in the reported case was caused by T-cell large granular lymphocytic leukemia, not dermatomyositis.

This perspective highlights evidence suggesting inflammation plays a significant role in male and female pattern hair loss, indicating that targeting inflammatory pathways may improve future therapeutic options.

This study found that adipose‐derived stem cells can restore skin barrier function and inhibit photoaging-related responses in UVB-irradiated mice, suggesting a potential therapeutic role in managing skin photoaging.

Light skin shows more inflammation from sun exposure than dark skin.

This article provides no abstract or new research findings on the androgenic pattern presentation of scarring and inflammatory alopecia.

In this study, researchers identified that certain inflammatory cytokines, including osteoprotegerin and leukemia inhibitory factor, are inversely associated with hypertrophic scar risk, whereas others like CDCP1, GDNF, and PD-L1 show a positive association, suggesting potential pathways for intervention in scar formation.

This review discusses the effects of photobiomodulation, particularly its potential to reduce inflammation in various conditions, but it does not report new clinical findings.

This study found that Wnt5a expression may suppress cell differentiation and induce an inflammatory response in HaCaT keratinocytes, which could be relevant to psoriasis development.

In this study, researchers found that using bioinspired nanovesicles derived from inflammation memory-activated epidermal stem cells effectively promoted healing in diabetic wounds by reprogramming neutrophils to an anti-inflammatory phenotype in both laboratory and animal models.

This study found that disrupting inflammasome signaling by eliminating caspase-1 and -11 in mice reduced skin inflammation and delayed the onset of disease, highlighting their role in skin disease pathogenesis.