Objective To investigate the effect of TREM2 on the inflammatory response at lesional sites of bullous pemphigoid (BP) by regulating macrophage efferocytosis. Methods We analyzed the expression of TREM2, the proportion and function of TREM2⁺ MΦs using the single cell RNA-sequencing data of lesional skin tissues from BP patients (NGDC# HRA003993). Bioinformatic analysis was performed to identify differentially expressed genes (DEGs), enriched signaling pathways, and functional differences between TREM2⁺ MΦs and TREM2^- MΦs,and the correlation between TREM2 expression and inflammatory factor levels in BP skin lesions. Additionally, H&E and immunofluorescence staining of C3 were used to evaluate the pathological changes in the lesional skin tissues. The number of TREM2⁺ MΦs in BP skin lesions was analyzed by immunofluorescence staining. Finally, Bone marrow-derived macrophages (BMDMs) from (wild type, WT) and Trem2 knockout (Trem2 KO) mice were cultured in vitro. Flow cytometry was used to assess the efferocytic capacity of macrophages and to determine the effect of TREM2 expression on apoptotic cell clearance. Results The lesional skin of BP patients showed typical clinical and pathological features of this disease. Single-cell transcriptomic analysis and immunofluorescence staining revealed a significant increase in the number of TREM2⁺ MΦs in BP lesions compared to normal skin (P<0.001), indicating a marked enrichment of this cell population in BP lesions. Furthermore, the expression levels of the inflammatory cytokines, IL-4 and IL-13, as well as the chemokines, CCL2 and CCL13, were significantly higher in BP lesional tissues and blister fluid than in normal skin (P<0.01), and their expression levels correlated positively with TREM2 expression. For cellular phenotype, TREM2⁺ MΦs in BP lesional tissues expressed monocyte markers (CD14 and FCGR3A) and M2-type macrophage markers (CD163 and MRC1), suggesting potential immunomodulatory functions. Functional analyses showed that TREM2⁺ MΦs exhibited significant enrichment of genes associated with efferocytosis pathways and demonstrated significantly enhanced efferocytic capacity compared with TREM2^- MΦs (P<0.01). Moreover, correlation analysis indicated that TREM2 expression tended to correlate positively with IL-10 (P=0.08) and negatively with IL-18 (P=0.01) and IL-33 (P=0.09), suggesting that TREM2^- MΦs may suppress local inflammation through efferocytosis.C。。。onclusion The increased TREM2⁺ MΦs in BP lesional tissues may suppress inflammatory responses through efferocytosis.

Objective To investigate the distribution and drug resistance profiles of multidrug-resistant organisms (MDROs) in skin wounds of inpatients in the Department of Dermatology, and to explore corresponding nursing strategies for prevention and control. Methods Clinical data of 149 inpatients with MDRO-infected skin wounds were retrospectively collected from the Hospital of Dermatology, Chinese Academy of Medical Sciences, between January 2020 and April 2025. Data were extracted via the hospital’s nosocomial infection management system. Demographics, underlying dermatoses, pathogen distribution, sampling sites, and antimicrobial susceptibility patterns were analyzed. Results Among the 149 patients, pemphigus (55 cases, 36.9%), bullous pemphigoid (25 cases, 16.8%), and mycosis fungoides (13 cases, 8.7%) were the most prevalent conditions. A total of 161 MDRO strains were isolated, including 109 (67.7%) Gram-positive bacteria, primarily methicillin-resistant Staphylococcus aureus (MRSA), multidrug-resistant Staphylococcus epidermidis, and multidrug-resistant Staphylococcus haemolyticus; and 52 (32.3%) Gram-negative bacteria, predominantly multidrug-resistant Klebsiella pneumoniae, Escherichia coli, and Proteus mirabilis. The most common sampling sites were the limbs (72 cases, 44.7%), followed by the trunk (55 cases, 34.2%) and the head, face, and neck (11 cases, 6.8%). MRSA showed high resistance rates to penicillin (98.8%), oxacillin (85.4%), and clindamycin (59.8%). Multidrug-resistant S. epidermidis exhibited high resistance rates to penicillin (94.4%), oxacillin (83.3%), and erythromycin (66.7%). Multidrug-resistant K. pneumoniae and E. coli showed high resistance rates against ceftriaxone (88.2% and 100%, respectively) and cefazolin (82.4% and 100%, respectively). Conclusions MDRO infections in dermatology inpatients primarily affect patients with compromised skin barrier, particularly those with pemphigus, bullous pemphigoid, and mycosis fungoides. The predominant Gram-positive MDROs are MRSA and S. epidermidis, while the predominant Gram-negative MDROs are K. pneumoniae and E. coli. The most common sites of MDRO infections are the limbs and trunk. Gram-positive MDROs demonstrate high resistance rates to penicillin, oxacillin, clindamycin, and erythromycin, whereas Gram-negative MDROs show high resistance rates to ceftriaxone, cefazolin, and nitrofurantoin.

Objective To assess the therapeutic effectiveness and safety profile of Xeligekimab in patients with moderate-to-severe psoriasis. Methods Thirty-eight patients with moderate-to-severe plaque psoriasis were enrolled. Patients received subcutaneous injections of Xeligekimab (200 mg) once every 2 weeks during the first 12 weeks, followed by once every 4 weeks for a total treatment duration of 16 weeks. The psoriasis area and severity index (PASI), physician global assessment (PGA), and dermatology life quality index (DLQI) were evaluated at baseline and at weeks 4, 8, 12, and 16. Adverse reactions were recorded throughout the study. Results Thirty-seven patients completed the 16-week follow-up, while one patient withdrew due to injection-site reactions and personal reasons. At week 16, the response rates for PASI 75, PASI 90, and PASI 100 were 100%, 86.49%, and 59.46%, respectively. The proportion of patients achieving a PGA score of 0 or 1 was 97.30%. The DLQI score improved significantly from a baseline of 13.49±5.81 to 0.51±0.90 at week 16. No serious adverse reactions occurred in any of the 37 patients.C。。。onclusion Xeligekimab significantly improves skin lesions and quality of life in patients with moderate-to-severe plaque psoriasis, demonstrating a favorable overall safety profile.

Objective To analyze the clinical characteristics, current management and trends of patients with localized scleroderma (LS), aiming to improve the understanding of this disease. Methods Clinical data of LS patients diagnosed at Dermatology Hospital, Southern Medical University between January 2019 and December 2024 were collected. A cross-sectional analysis was conducted to describe patients’ demographics (sex, age), clinical manifestations (lesion type, distribution, disease duration), laboratory findings, and treatment regimens. The differences in lesion site and treatment strategy across different clinical subtypes were evaluated. Results A total of 448 LS patients were included, comprising 327 females and 121 males, with a median age at onset of 21 years (interquartile range: 9, 33), and a female-to-male ratio of 2.7 ∶1. The clinical subtypes of LS were predominantly plaque type (47.32%), followed by linear type (40.00%), and generalized type (10.71%). There was a significant variation in lesion distribution across these different subtypes (P<0.001). Only a small proportion of patients (1.56%) reported clinical symptoms such as joint limitation or numbness. Treatment approaches varied with the phase of the disease, with patients in the active phase more frequently receiving a combination of topical corticosteroids, calcineurin inhibitors, and phototherapy compared to those in the inactive phase (P<0.05). Additionally, Janus kinase (JAK) inhibitors were utilized relatively often in the clinical management of LS. Conclusions LS predominantly affects children aged 0-12 years and young to middle-aged adults aged 19-40 years. Clinical manifestations are heterogeneous. Systemic therapy is more widely applied in patients with active disease, and novel targeted agents, particularly JAK inhibitors, are increasingly utilized in clinical practice. However, their long-term efficacy and safety require further investigation.

Objective To assess the serum granzyme B levels in patients with atopic dermatitis, and to analyze their association with disease severity and clinical characteristics. Methods Ninety patients with atopic dermatitis (AD) and 30 healthy controls were enrolled, and their serum specimens were collected. The ELISA assay was used to measure serum granzyme B levels, and their correlations with disease severity, IgE levels, eosinophil counts, and IL-18 were analyzed. Results Serum granzyme B levels were significantly elevated in AD patients compared with healthy controls (P<0.001) and positively correlated with SCORAD scores (P<0.001), eosinophil counts (P<0.05), and IL-18 levels (P<0.001). Granzyme B levels differed significantly among mild, moderate, and severe AD subgroups (P<0.001), with all pairwise comparisons reaching statistical significance (P<0.05 or P<0.001). No significant difference in granzyme B levels was observed between endogenous and exogenous AD (P>0.05). A unit increase (pg/mL) in granzyme B was associated with an average increase of approximately 14.28 units in IL-18 levels (P<0.001). Moreover, granzyme B was identified as an independent risk factor for AD severity, with an odds ratio (OR) greater than that of eosinophil counts (P<0.001). Logistic regression analysis revealed that both granzyme B and eosinophil counts were independent risk factors for AD severity (P<0.001). ROC curve analysis showed that the area under the curve (AUC) for granzyme B was 0.649, lower than the 0.826 for eosinophil counts. At the optimal cutoff values, the sensitivities of granzyme B and eosinophil counts were 37.8% and 65.6%, respectively, while both exhibited a specificity of 96.7%. Conclusions Serum granzyme B is significantly elevated in patients with atopic dermatitis and serves as an independent risk factor for disease severity. It is positively correlated with IL-18 levels and eosinophil counts. Although it exhibits high specificity, its relatively low sensitivity suggests that it may be more suitable as an ancillary marker for disease assessment rather than as a standalone screening tool.

Objective To investigate the treatment patterns and disease burden of patients with moderate-to-severe plaque psoriasis. Methods A retrospective analysis was conducted on the general demographics, clinical characteristics, treatment patterns, clinical outcomes, direct medical costs, and healthcare resource utilization (HCRU) of patients with moderate-to-severe plaque psoriasis treated at the Department of Dermatology, Hospital of Dermatology, Chinese Academy of Medical Sciences, and the Department of Dermatology, Beijing Friendship Hospital, Capital Medical University, from January 2018 to December 2021. Additionally, a questionnaire survey was administered to patients with moderate-to-severe plaque psoriasis visiting the dermatology departments of these two hospitals between October 2022 and March 2023 to collect data on their baseline characteristics and treatment history. Results A total of 1,102 patients were included in the retrospective analysis, with a mean age of 44.90±14.64 years, of whom 77.22% were male and 22.78% were female.During the observation period, 87.84% of patients discontinued systemic therapy. The average annual outpatient visits per patient were 6.47±5.21.Among inpatients (n=118), the average annual duration of hospital stay was 9.29 days, and the average direct medical cost was (371.09 ± 141.56) RMB per month. The cross-sectional survey included 380 patients, of whom 62.17% received only topical treatment and 17.72% were treated with biologics.Additionally, 75.26% of patients had fully adhered to their treatment plan in the past six months. However, 42.11% of patients expressed dissatisfaction or a neutral attitude toward treatment efficacy and safety. According to the EQ-5D-3L assessment results, nearly one-third of patients reported symptoms of anxiety or depression. Conclusions Patients with moderate-to-severe plaque psoriasis predominantly receive topical therapy, yet bear a substantial disease burden and experience poor health-related quality of life. It is recommended to further improve patient care and enhance disease management capabilities by increasing reimbursement rates under medical insurance schemes and developing standardized clinical practice guidelines.

We report a case of superficial CD34 positive fibroblast tumor. A 49-year-old woman had a subcutaneous mass on her upper right back for more than 2 years. Physical examination revealed a firm, non-tender, and poorly mobile nodule measuring 2.0 cm×1.5 cm, with an erythematous overlying skin. Histopathology showed a dermal neoplasm consisting of interlacing bundles of spindle cells in a whorled growth pattern and sparse mitotic activity. Immunohistochemical staining demonstrated CD34 (diffuse+), CK (focal+), Ki-67(5%+), Pan TrK(-), S-100(nerve+) and SMA(a little+). Diagnosis: Superficial CD34-positive fibroblast tumor. The mass was completely resected and no recurrence or metastasis was observed during 9 months of follow-up.

We report a case of talaromycosis diagnosed with the assistance of reflectance confocal microscopy (RCM) and dermoscopy. A 38-year-old man presented with a one-week history of asymptomatic papules and nodules on the face. Dermatological examination revealed scattered or clustered skin-colored to erythematous papules and nodules ranging from rice grain to soybean size. The surface was smooth or umbilicated, with some lesions showing focal erosion covered by purplish-red hemorrhagic crusts. RCM examination showed that the spinous layer appeared thinned with widened dermal papillae. The superficial dermis contained highly refractive fine granular material that aggregated into globular structures resembling “grapes or mulberries”. Dermoscopy revealed a light red or skin-colored background with focal distribution of dotted and thin linear vessels, along with adherent yellowish-brown scales. Some lesions showed patchy purplish-red spots. Based on these RCM and dermoscopic findings, an initial suspicion of Talaromyces marneffei infection was raised. The patient was treated with oral itraconazole tablets, resulting in gradual regression of the lesions. At follow-up, a skin biopsy was performed. Histopathology showed mild hyperkeratosis and epidermal attenuation with numerous blue-gray spores in the superficial dermis, some forming clusters. Periodic acid-Schiff (PAS) staining highlighted red-stained spores, some displaying a central transverse septum. Fungal culture confirmed the diagnosis of Talaromyces marneffei(formerly Penicillium marneffei). The patient showed excellent clinical response to itraconazole. After two months of follow-up, the skin lesions had almost completely resolved. The patient was subsequently lost to follow-up.

Research has found that both psoriasis and obesity exhibit disturbances in energy metabolism, such as impaired fatty acid β-oxidation. They share significant elevations in the levels of branched-chain amino acids and aromatic amino acids, constituting characteristic metabolic reprogramming of amino acids, accompanied by remodeling of complex lipid homeostasis involving phospholipids, sphingolipids, and steroid metabolism. In-depth analysis indicates that these shared metabolic abnormalities form a “metabolic-inflammatory” vicious cycle by persistently activating key inflammatory pathways such as mTOR and NF-κB and perturbing inflammatory regulatory hubs like tryptophan-kynurenine metabolism. This cycle acts as a “metabolic bridge” linking the two diseases. Animal studies further suggest that saturated fatty acid / bile acid metabolism disorders and neutrophil extracellular traps (NETs) are key links in the aggravation of psoriasis by obesity. These findings provide new integrated perspectives for understanding the comorbidity mechanisms of psoriasis and obesity, and also offer a theoretical basis for future discovery of comorbidity biomarkers and development of intervention strategies targeting shared metabolic pathways. This article aims to systematically review the potential metabolic basis of the comorbidity between psoriasis and obesity by integrating metabolomics data.

The P2X7 receptor (P2X7R) and the NLRP3 inflammasome constitute a key signaling pathway in the regulation of inflammatory responses and play a critical role in various inflammatory skin diseases. Upon activation by extracellular ATP, P2X7R mediates the activation of NLRP3 inflammasome through transmembrane ion signaling, thereby driving downstream inflammatory responses. This pathway exhibits heterogeneous regulatory patterns across different diseases, including the formation of an ATP-IL-23 positive feedback loop in psoriasis, a LL37-centered interactive network in rosacea, as well as positive feedback amplification involving IL-17/IL-1β in hidradenitis suppurativa and TNF-α in Behçet’s disease. This review systematically summarizes the mechanistic roles and targeted therapeutic strategies of P2X7R and NLRP3 in inflammatory skin disorders, aiming to provide a theoretical basis and translational perspective for further mechanistic research and therapeutic development.

Immunological skin diseases are a group of autoimmune disorders characterized by complex pathogenesis. Recent research has identified targeting metabolism-related genes and their pathways as a promising therapeutic strategy. The CYP gene family can modulate the AHR-CYP axis and vitamin D metabolism to suppress immune hyperactivation and optimize drug efficacy. The NR family, centered on nuclear receptors such as PPAR and LXR, orchestrates lipid metabolism and cell differentiation to achieve the dual benefits of anti-inflammation and barrier repair. Interventions targeting ABC transporters can influence drug transport, thereby affecting the therapeutic efficacy and toxicity of medications. The SLC family remodels glucose and amino acid metabolism to block the activation of immune cells such as Th17. Furthermore, the KLK family improves pruritus and barrier dysfunction by balancing proteolysis and the PAR2 pathway, while the SREBP family inhibits inflammasome activation through homeostatic regulation. This review systematically summarizes the latest research advances in these six major metabolism-related gene families in the treatment of immunological skin diseases, providing new perspectives for clinical therapy.