Immunologic Research最新文献

{"title":"The epidemiological trends of inflammatory bowel disease among women of reproductive age: a global analysis from 1990 to 2021.","authors":"Zhenzhen Fan, He Zhou, Lianlian Tian, Tong Wu, JiaQi Zhang, Junchao Lin, Chen Wang, Jindan He, LiuQing Zhao, Jie Chen, Jie Liang","doi":"10.1007/s12026-025-09658-x","DOIUrl":"https://doi.org/10.1007/s12026-025-09658-x","url":null,"abstract":"<p><p>This study aimed to evaluate the global burden of inflammatory bowel disease (IBD) among women of reproductive age (15-49 years) from 1990 to 2021, analyze its association with socio-demographic index (SDI), and identify age-period-cohort (APC) effects to inform region-specific public health strategies. Using data from the Global Burden of Disease (GBD) 2021 study, we assessed age-standardized incidence (ASIR), prevalence (ASPR), mortality (ASMR), and disability-adjusted life years (ASDR) across 204 countries. Statistical analyses included Pearson correlation to evaluate SDI associations, decomposition analysis to quantify burden drivers, and APC modeling to disentangle age, period, and cohort effects. In 2021, the global ASIR, ASPR, ASMR, and ASDR for IBD in women of reproductive age were 4.38, 45.90, 0.50, and 17.75 per 100,000, respectively. The health burden of IBD in women of reproductive age varies by region. Australasia has the highest ASIR and ASPR globally, while these metrics are lowest in Central Latin America. Western Europe exhibits the highest ASMR, whereas Oceania has the lowest. In terms of ASDR North America, with its higher income, bears the heaviest burden, while Oceania experiences the lightest. Furthermore, APC analysis revealed age-specific risks peaking at 45-49 years, and significant cohort effects in middle/low-SDI regions, where post-1977 birth cohorts showed elevated incidence. Period effects highlighted diverging trends: stable incidence in high-SDI regions vs. rising rates in mid-SDI regions due to urbanization and lifestyle shifts. The IBD burden among reproductive-aged women is rising disproportionately, shaped by SDI gradients and demographic transitions. High-SDI regions require strategies targeting aging populations and comorbidities, while low/middle-SDI regions need investments in early diagnosis and equitable care.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"101"},"PeriodicalIF":3.3,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HBV infection upregulates GP73 expression to promote liver fibrosis by enhancing ER stress via the Smad2 pathway.","authors":"Ying He, Lianying Cai, Liu Liu, Yuxu Zhang, Lu Si, Qiuchen Cheng, Shuangyan Luo","doi":"10.1007/s12026-025-09656-z","DOIUrl":"https://doi.org/10.1007/s12026-025-09656-z","url":null,"abstract":"<p><p>Endoplasmic reticulum (ER) stress induced by hepatitis B virus (HBV) infection is associated with the development of liver fibrosis. Golgi protein 73 (GP73) is increased during HBV infection. Nevertheless, whether GP73 during HBV infection mediates ER stress in liver fibrosis is still poorly understood. TGF-β1 was used to induce HepG2.2.15 cells to establish liver fibrosis cells model. GP73 expression was evaluated using qRT-PCR analysis and Western blot. HepG2.2.15 cells viability and proliferation were assessed via CCK-8 assay and EdU assay, respectively. The protein levels of α-SMA, fibronectin, collagen I and collagen III for liver fibrosis, GRP78, p-PERK, p-eIF2α, ATF4 and CHOP for ER stress, as well as p-Smad2 and Smad2 were evaluated by Western blot. TGF-β1 incubation obviously elevated GP73 expression, while GP73 knockdown reduced the GP73 levels in HBV-transfected HepG2215 cells. GP73 knockdown reversed the effects of TGF-β1 exposure on HepG2.2.15 cells viability and proliferation. The protein levels of liver fibrosis marker, ERS marker and p-Smad2 were remarkably increased following TGF-β1 stimulation, which were counteracted by GP73 silence or the application of 4-phenylbutyric acid (4-PBA). However, these results were opposite after tunicamycin (TM) treatment. In conclusion, knockdown of GP73 potentially impeded the advancement of liver fibrosis via mediating ERs through Smad2 signal pathway.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"100"},"PeriodicalIF":3.3,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunomodulatory activity of 4-(Benzyloxy)phenol facilitates intracellular mycobacterial clearance through p53 mediated IL-35 signaling dependent JAK1/STAT3 pathway in human macrophages.","authors":"Lincoln Naik, Salina Patel, Mousumi Das, Dev Kiran Nayak, Pramathesh Kumar Dandsena, Mustafeez Ali Quaderi, Ashish Kumar, Amit Mishra, Ramandeep Singh, Abtar Mishra, Rohan Dhiman","doi":"10.1007/s12026-025-09657-y","DOIUrl":"https://doi.org/10.1007/s12026-025-09657-y","url":null,"abstract":"<p><p>Mycobacterium tuberculosis (M. tuberculosis), the causative agent of tuberculosis (TB), modulates host immune responses by regulating various cytokines. Precise regulation of these cytokines renders the host pathogen-free, whereas their dysregulation increases the susceptibility to infection. Hence, induction of host protective cytokines using immunomodulators to promote M. tuberculosis clearance has a rewarding impact in the context of TB treatment. This study explored the immunomodulatory activity of 4-(Benzyloxy)phenol (4-BOP) in mycobacteria infected differentiated THP-1 cells through IL-35 (an anti-inflammatory cytokine) production. Initially, we observed an increased mRNA and protein level expression of IL-35 and its cognate receptor upon 4-BOP treatment in mycobacteria-infected dTHP-1 cells. IL-35 receptor activation further led to phosphorylation of JAK1/STAT3, culminating in increased phagosome-lysosome fusion through elevation of intracellular Ca²⁺ level. Blocking IL-35 receptors using siRNA-mediated approach against IL-12Rβ2 and gp130 or the JAK1/STAT3 associated signaling with specific inhibitors like Baricitinib and Stattic promoted the intracellular mycobacterial survival by compromising Ca²⁺-phagosome-lysosome fusion pathway. Further, we identified a direct regulatory role of p53 (known to be activated by 4-BOP) on IL-35 production, and inhibition of p53 using PFT-α surprisingly abrogated the IL-35 mediated signaling axis. Collectively, our results demonstrated a host defensive role of 4-BOP-induced Il-35 signaling in mycobacteria-infected dTHP-1 cells through the JAK1/STAT3 mediated Ca²⁺-phagosome-lysosome fusion pathway. These results suggest that 4-BOP may serve as a potent HDT candidate for regulating inflammation and enhancing host defense in TB infection.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"99"},"PeriodicalIF":3.3,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High expression of signal regulatory protein beta 2 marks a favourable prognostic AML subgroup and associates with increased sensitivity to phagocytosis.","authors":"Nienke Visser, Nisha K van der Meer, Yuan He, Gerwin Huls, Jan Jacob Schuringa, Edwin Bremer","doi":"10.1007/s12026-025-09659-w","DOIUrl":"10.1007/s12026-025-09659-w","url":null,"abstract":"<p><p>Acute myeloid leukaemia is an aggressive hematologic malignancy that remains exceedingly difficult to treat despite recent advancements. High expression of CD47 on leukemic blasts interacts with the inhibitory receptor SIRP-alpha (SIRP-α) on innate immune cells, resulting in a strong \"don't eat me\" signal. Therefore, identifying AML patients who could benefit from immune-targeted therapies is crucial SIRP-β2 is predominantly expressed in myeloid cells and positively regulates innate anticancer immunity. Furthermore, endogenously expressed SIRP-β2 potentiates cancer cell trogocytosis by granulocytes. Here, we delineate the role of SIRP-β2 in AML. High expression of SIRP-β2 is independently associated with favorable overall survival (OS) and event free survival (EFS) independent of the ELN intermediate risk group. SIRP-β2 is more prevalent in the more committed FAB M4 and M5 subgroups. SIRP-β2 is also expressed on normal myeloid cells in patient samples, with higher expression on tumor-suppressive M1 macrophages than on adverse prognostic and tumor-supportive M2 macrophages. In line with this, co-culture of macrophages/neutrophils with ectopically expressed SIRP-β2 tumor cells results in an increased phagocytosis/trogocytosis treated with anti-CD47. These data indicate that AML patients with high SIRP-β2 AML expression could significantly benefit from innate immune-targeting therapies such as CD47 immune checkpoint inhibitor.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"98"},"PeriodicalIF":3.3,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12198062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144484115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Statins and adhesion molecules: a review of a novel pleiotropic property of statins.","authors":"Mahvash Sadeghi, Sajad Dehnavi, Sanaz Keshavarz Shahbaz, Khadijeh Koushki, Alexandra E Butler, Tannaz Jamialahmadi, Amirhossein Sahebkar","doi":"10.1007/s12026-025-09653-2","DOIUrl":"https://doi.org/10.1007/s12026-025-09653-2","url":null,"abstract":"<p><p>Statins were introduced as lipid-lowering agents that inhibit 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG CoA) reductase; they are commonly administered to reduce cholesterol levels for cardioprotective purposes. Further studies suggested that statins have cholesterol-reducing-independent properties and exert pleiotropic therapeutic properties, including antioxidant, anti-inflammatory, anti-fibrotic, neuroprotective, and other beneficial effects. Adhesion molecules, including selectins, integrins, cadherins, CD44, and the immunoglobulin superfamily (IgSF) members, are essential mediators for those biological functions. The current review discusses studies performed in in vitro and in vivo in physiological and pathological models focusing on adhesion molecules such as Lymphocyte function-associated antigen-1 (LFA-1), macrophage-1 antigen (Mac-1), P-selectin, E-selectin, very late activation antigens-4 (VLA-4), and nectins that are therapeutically targeted by different types of statins and that highlight the potential therapeutic utility of statins for diseases other than cardiovascular disease.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"97"},"PeriodicalIF":3.3,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144316829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The relationship between self-reported immune fitness and salivary immune biomarker concentrations.","authors":"Emina Išerić, Pauline A Hendriksen, Guusje A Ulijn, Marit Zuurveld, Aurora Jae van de Loo, Johan Garssen, Joris C Verster","doi":"10.1007/s12026-025-09654-1","DOIUrl":"10.1007/s12026-025-09654-1","url":null,"abstract":"<p><p>Immune fitness refers to the body's ability to respond to health challenges by activating an appropriate immune response. Perceived immune fitness can be assessed using a single-item scale ranging from 0 (very poor) to 10 (excellent). The aim of the current study (n = 29 healthy volunteers) was to evaluate the relationship between perceived immune fitness and immune biomarker concentrations in saliva. Hourly assessments of immune fitness were made throughout the day (09:30 - 15:30), and saliva samples were collected accordingly. The concentrations of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α) were determined using multiplex immunoassay. While immune fitness scores remained stable during the day, biomarker assessments showed some fluctuations. For IL-6, significant negative correlations were found between IL-6 concentration at 10:30 and immune fitness scores at 10:30 (r = -0.512), 11:30 (r = -0.383), and 12:30 (r = -0.443), and between the IL-6 concentration and immune fitness score at 15:30 (r = -0.704). For IL-8, significant correlations were found between IL-8 concentration at 10:30 and immune fitness scores at 10:30 (r = -0.480), 12:30 (r = -0.456), and 14:30 (r = -0.429). For TNF-α, significant positive correlations were found between TNF-α concentration at 13:30 and immune fitness scores at 13:30 (r = 0.517) and 14:30 (r = 0.477). No significant correlations were found between immune fitness and IL-1β. In conclusion, immune fitness scores remained stable throughout the day, and were significantly associated with salivary concentrations of IL-6, IL-8, and TNF-α at certain time points.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"96"},"PeriodicalIF":3.3,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12159093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Staphylococcus aureus α-hemolysin induces DNA methylation changes in human Th1 cells.","authors":"Iwona Karwaciak, Joanna Pastwińska, Anna Sałkowska, Kaja Karaś, Marta Sobalska-Kwapis, Jarosław Dastych, Marcin Ratajewski","doi":"10.1007/s12026-025-09647-0","DOIUrl":"10.1007/s12026-025-09647-0","url":null,"abstract":"<p><p>α-Hemolysin is one of the most dangerous virulence factors produced by Staphylococcus aureus. Among the immune cells that respond to this pathogenic bacterium, Th1 lymphocytes play a critical role. In our study, we investigated the impact of α-hemolysin on the methylation of the Th1 cell genome. Our findings revealed that α-hemolysin upregulates HELLS and DNMT3A expression while downregulating DNMT3L expression at the protein level. Whole-genome bisulfite sequencing analysis revealed significant alterations in DNA methylation, particularly in regions outside CpG sequences. These results suggest that bacterial proteins can act as potent epigenetic modulators in human cells, influencing their activity, plasticity, and phenotype.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"95"},"PeriodicalIF":3.3,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12159126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144266075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FOXO1 contributes to cigarette smoke condensate-induced cellular senescence and fibrosis in lung fibroblasts through activating the TGF-β1/Smad2/3 signaling pathway.","authors":"Mengning Zheng, Guohang Yuan, Jing Han, Jiayi Li, Youjun Jiang, Zhaoxia Li, Yang Yao","doi":"10.1007/s12026-025-09646-1","DOIUrl":"https://doi.org/10.1007/s12026-025-09646-1","url":null,"abstract":"<p><p>Cigarette smoking is the most dominant factor contributing to chronic obstructive pulmonary disease (COPD). Fibroblasts are sensitive to cellular injury induced by cigarette smoke condensate (CSC). This study was devoted to discovering the potential target and exploring its regulatory mechanism in CSC-induced human fibroblasts. Network pharmacological analysis for differential genes in CSC-induced lung fibroblasts MRC5 was performed by a bioinformatics platform. COPD in vitro was induced by CSC in MRC5. The protein expression was analyzed by western blotting. Cellular senescence was tested by senescence-associated β-galactosidase assay and protein detection. Oxidative indexes were examined by corresponding kits. Inflammatory factors were detected using enzyme-linked immunosorbent assay. Markers associated with the TGF-β1/Smad2/3 pathway and fibrosis were also determined via western blotting. FOXO1 and TGF-β1 binding was analyzed by ChIP assay. An animal model was established to explore the effect of FOXO1 in vivo. Gene Ontology (GO) analysis of the differential genes in CSC-induced MRC5 cells indicated gene functions and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed the top 10 pathways. Forkhead box O 1 (FOXO1) was an upregulated gene in the cellular senescence pathway. Cell function assays suggested that FOXO1 knockdown restrained CSC-induced cellular senescence, oxidative stress, and inflammation in MRC5. FOXO1 downregulation inactivated the TGF-β1/Smad2/3 pathway and suppressed fibrosis markers in CSC-treated MRC5 cells. FOXO1 directly interacted with TGF-β1 promoter and facilitated cell senescence by upregulating TGF-β1. TGF-β1 abolished the suppression of TGF-β1/Smad2/3 pathway and fibrosis caused by FOXO1 knockdown. FOXO1 promoted COPD in mice by regulating the TGF-β1/Smad2/3 pathway. The obtained evidence affirmed that FOXO1 contributed to CSC-induced cellular senescence and fibrosis by promoting TGF-β1 transcription to mediate the TGF-β1/Smad2/3 pathway, indicating an important mechanism in the pathogenesis of COPD.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"94"},"PeriodicalIF":3.3,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144266074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The mechanism of p38 MAPK, NF-κB, and IL-6 in T-2 toxin and/or selenium deficiency induced spleen injury.","authors":"Xiang Xiao, Rongqi Xiang, Jiaxin Liu, Ziwei Guo, Haobiao Liu, Xue Lin, Miaoye Bao, Viscardi Angelo, Jing Han","doi":"10.1007/s12026-025-09650-5","DOIUrl":"https://doi.org/10.1007/s12026-025-09650-5","url":null,"abstract":"<p><p>Both T-2 toxin and selenium (Se) cause immune impairment in the spleen, but the mechanism of their occurrence is not clear. In this experiment, the Se content of the spleen was tested by atomic fluorescence spectrometry after a 12-week intervention in Sprague-Dawley (SD) rats, divided into normal, normal + T-2 toxin (10 ng/g), normal + T-2 toxin (100 ng/g), low Se, low Se + T-2 toxin (10 ng/g), and low Se + T-2 toxin (100 ng/g) groups. The pathological changes and fibrosis of spleen tissue were observed using hematoxylin-eosin (HE) staining and Masson staining, respectively. Mitogen-activated protein kinase p38 (p38 MAPK), phosphorylated protein-38 (P-p38 MAPK), nuclear factor kappa-B (NF-κB), and interleukin-6 (IL-6) expression levels in spleen tissues were analyzed by Western blotting (WB) and immunohistochemistry (IHC) staining. This study found that both Se deficiency and T-2 toxin induced inflammatory injury and fibrotic changes in rat spleen, but low selenium and low selenium combined with T-2 toxin intervention showed more intense splenic injury. Se deficiency combined with T-2 toxin intervention aggravated spleen injury, and the mechanism of occurrence involved an increase in the inflammatory injury in the spleen by elevating the expression levels of p38 MAPK, NF-κB, and IL-6 in rat spleen.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"93"},"PeriodicalIF":3.3,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deucravacitinib as a monotherapy for concurrent management of psoriasis and chronic spontaneous urticaria.","authors":"Xiaoying Zhang, Chenxi Zhang, Jiali Liang, Yifei Liu, Bichun Xu, Changxing Li","doi":"10.1007/s12026-025-09649-y","DOIUrl":"https://doi.org/10.1007/s12026-025-09649-y","url":null,"abstract":"<p><p>Patients with autoimmune diseases are susceptible to developing a second autoimmune disorder. Psoriasis, a common autoimmune disease, frequently occurs alongside other autoimmune conditions in some individuals. We report the case of a young female patient diagnosed with plaque psoriasis, initially treated with secukinumab, and achieved complete skin clearance at 12 weeks. However, she experienced a decline in the efficacy of secukinumab, with recurrence of symptoms and subsequent development of chronic spontaneous urticaria (CSU) and was switched to treatment with deucravacitinib, an oral, selective, allosteric tyrosine kinase 2 inhibitor. The use of deucravacitinib resulted in a favorable therapeutic outcome, effectively managing both psoriasis and CSU 12 weeks after treatment. This case highlights the potential of deucravacitinib as a novel monotherapy for patients with both psoriasis and CSU.</p>","PeriodicalId":13389,"journal":{"name":"Immunologic Research","volume":"73 1","pages":"92"},"PeriodicalIF":3.3,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}