Mengguo Liu

Fox-Fordyce disease (apocrine miliaria) is a classic apocrine gland-related inflammatory skin disorder, and most previously documented clinical cases present with severe pruritus. We report a rare case of bilateral axillary Fox-Fordyce disease in a 14-year-old adolescent girl, distinguished by prominent perifollicular foam histiocyte aggregation with co-expression of pan-macrophage marker CD68 and scavenger receptor CD163. A full panel of eight immunohistochemical markers verified negative expression of multiple lineage-specific biomarkers in these foam cells. The patient presented with six months of painless, non-pruritic symmetric follicular papules confined to bilateral axillae, without burning sensation, exudation, or lesions on other apocrine-rich body sites. Specimens obtained via conventional skin biopsy were subjected to histopathological testing, which revealed follicular keratotic plugs, follicular epithelial hyperplasia, mild epidermal spongiosis, dilated hyperactive apocrine glands, and mixed perifollicular inflammatory infiltrates consisting of lymphocytes, plasma cells and abundant foam-like histiocytes. Immunohistochemical testing confirmed the foam cells were CD163(+) and CD68(+), while S100, SMA, EMA, Langerin, ALK1 and CD34 were all negative, consistent with the pathognomonic perifollicular xanthomatosis characteristic of Fox-Fordyce disease. This case objectively describes the unique local inflammatory cell phenotype dominated by CD163/CD68 double-positive foam histiocytes within non-pruritic Fox-Fordyce lesions. We systematically discuss the correlation between apocrine gland secretory activity, follicular stromal inflammatory infiltration and foam histiocyte formation, analyze the differential diagnostic value of this CD163/CD68 immunophenotype across apocrine inflammatory dermatoses, and explore the research value of CD163+/CD68+ foam histiocytes as tissue-resident antigen-presenting cells in sterile cutaneous inflammation.

Keloid, as a unique form of pathological scar, involves complex interactions across multiple dimensions in its pathogenesis, including genetic susceptibility, epigenetic regulation, immune microenvironment disorders, metabolic reprogramming, abnormal mechanical force transduction, and fine-tuning by non-coding RNAs. At the genetic level, alleles such as HLA-DRB1*15, HOX gene family, and high-frequency mutation genes including MUC4 constitute the foundation of congenital susceptibility; at the epigenetic level, reduced DNA methylation and imbalanced m6A modification promote fibrosis by regulating target genes such as COL1A1. In core signaling pathways, TGF-β/Smad, MAPK/ERK, PI3K/AKT/mTOR, and Wnt/β-catenin pathways form a cross-talk network, driving persistent activation of fibroblasts and excessive extracellular matrix deposition. Characteristics of the immune microenvironment include M2-like macrophage polarization, Th17/IL-17 axis activation, and chronic low-grade inflammation maintained by inflammatory factor networks such as CXCL12. Regarding metabolic reprogramming, keloid cells exhibit “Warburg effect” features, prioritizing aerobic glycolysis while suppressing oxidative phosphorylation, alongside ferroptosis resistance and abnormal sphingolipid metabolism. Mechanical forces trigger the opening of mechanosensitive PIEZO1 ion channels, inducing abnormal calcium influx and subsequent YAP/TAZ nuclear translocation, which creates a self-amplifying vicious cycle alongside elevated matrix stiffness. Furthermore, lncRNAs, circRNAs, and miRNAs finely regulate the fibrotic process through competing endogenous RNA (ceRNA) networks and m6A modification-dependent mechanisms. The integration of these multidimensional mechanisms provides a theoretical basis for developing multi-target combination therapeutic strategies. Future research should promote the application of precision medicine in keloid management through multi-omics integration and artificial intelligence algorithms. Microenvironment; Metabolic reprogramming; Mechanical force transduction.

Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by immune dysregulation, microvascular damage, and multi-organ fibrosis. Recent breakthroughs in single-cell and spatial multi-omics technologies have profoundly revealed the high heterogeneity of the SSc immune microenvironment, including extensive aberrant activation of innate immunity (e.g., dendritic cells, macrophages, neutrophils) and adaptive immunity (T cells, B cells), and their interaction with fibroblasts and endothelial cells through an “immune-stromal-vascular” network that collectively drives the fibrotic process. These findings have advanced disease subtyping based on molecular features (e.g., inflammatory, fibrotic) and the development of precision therapeutic strategies. Emerging therapies targeting the IL-6 receptor (tocilizumab), B cells (rituximab, belimumab, CAR-T), the JAK-STAT pathway (tofacitinib, baricitinib), and T-cell co-stimulation (abatacept) have shown potential to improve disease progression in clinical studies. However, heterogeneity in treatment response, difficulty in reversing fibrosis, and the lack of biomarkers remain current challenges. Future efforts require integrating multi-omics and artificial intelligence technologies to build dynamic predictive models, promoting multi-target combination and individualized therapies, ultimately aiming for early intervention and long-term remission in SSc.

Keloids and bullous pemphigoid (BP) are two clinically and pathophysiologically distinct dermatologic disorders – the former involves abnormal scar formation due to excess collagen deposition, while the latter is an autoimmune blistering disease. We report a case of a 67-year-old man with a 19-year history of abdominal keloids and the subsequent appearance of vesicular skin lesions. Histopathologic examination revealed both keloidal fibrosis and subepidermal blister formation. Serum testing demonstrated elevated anti-BP180 antibody levels. Initial treatment with topical and systemic agents, including neomycin, glycyrrhizin, spironolactone, and minocycline, resulted in limited improvement. Subsequently, dupilumab – a monoclonal antibody against the interleukin (IL)-4 receptor α – was introduced. After two months of dupilumab therapy, the vesicular lesions resolved, keloids stabilized, serum anti-BP180 antibody levels normalized, and the Dermatology Life Quality Index (DLQI) score decreased from 11 to 2.

Background: The use of dermatoscopes is constantly increasing globally, but to date, there are no studies on the use of dermatoscopes by Chinese dermatologists.Objective: To determine factors influencing the use of dermatoscopes in China.Methods: A web‐based questionnaire was designed by the Department of Dermatology at Huashan Hospital affiliated with Fudan University and was published online via the Shanghai Wheat Color Intelligent Technology Company, China. In 2019 and 2022, 1581 and 1507 dermatologists, respectively, were recruited and completed the questionnaire online.Results: In China, the application rate of dermatoscopy is higher in eastern provinces than in western and remote areas. The proportion of doctors from public tertiary hospitals is the highest, with females being the majority. The age range of 30–40 years has the highest proportion, the proportion of doctors with professional titles of attending physician or above is the highest, and the proportion of doctors with a bachelor's degree or above is the highest.Conclusions: By improving the education and professional standards of doctors, providing more training opportunities, simplifying access, and promoting dermatoscopy in grassroots hospitals, we can increase the confidence of dermatologists in the use of dermatoscopy.

B cells play a central role in the pathogenesis of systemic sclerosis (SSc). Most B-cell studies have focused on their pathological role as antibody producers. However, in addition to immunoglobulin secretion, these cells have a wide range of functions in the immune response, including antigen presentation to T cells and cytokine production. Importantly, not all B-cell subsets promote the immune response. Regulatory B cells (Bregs) attenuate inflammation and contribute to the maintenance of immune tolerance. However, effector B cells (Beffs) positively modulate the immune response through the production of various cytokines. In SSc, Bregs are insufficient and/or dysfunctional. B-cell-targeting biologics have been trialled with promising results in the treatment of SSc. These therapies can affect Bregs or Beffs, which can potentially limit their long-term efficacy. Future strategies might involve the modulation of effector B cells in combination with the stimulation of regulatory subsets. Additionally, the monitoring of individual B-cell subsets in patients may lead to the discovery of novel biomarkers that could help predict disease relapse or progression. The purpose of this review is to summarize the relevant literatures and explain how Bregs and Beffs jointly participate in the pathogenesis of SSc.