Clinical and experimental immunology最新文献

{"title":"CD137 deficiency patients: two new patients and review of the literature.","authors":"Zehra Genc Ozbay, Busra Kocali, Deniz Ilgun Gurel, Ismail Yaz, Baris Ulum, Dilek Aktas, Ece Ozogul, Elif Soyak Aytekin, Saliha Esenboga, Aysegul Uner, Baris Kuskonmaz, Deniz Cagdas","doi":"10.1093/cei/uxag021","DOIUrl":"10.1093/cei/uxag021","url":null,"abstract":"<p><p>CD137 (4-1BB, TNFRSF9) plays a crucial role in T-cell activation, proliferation, and antiviral immunity. Biallelic TNFRSF9 variants cause CD137 deficiency, a rare inborn error of immunity characterized by Epstein-Barr virus (EBV)-induced hemophagocytic lymphohistiocytosis (HLH) and lymphoproliferation/malignancy. In this study, we aimed to characterize the clinical, immunological, and genetic spectrum of CD137 deficiency to provide insights into patient management. We recruited two patients carrying the same homozygous large deletion encompassing exons 1-6 of the TNFRSF9 gene and reviewed previously reported cases. The genetic defect was identified by whole-exome sequencing and confirmed by multiplex ligation-dependent probe amplification. Reported variants included missense, splice-site, and frameshift variants, large deletions, and compound heterozygous variants. A total of 14 patients, including the two newly reported cases, exhibited recurrent sinopulmonary infections and EBV viremia. HLH occurred in four patients (28.5%), including both newly reported patients, while lymphoma developed in seven patients (50%). Most patients were of Middle Eastern origin, and parental consanguinity was documented in 12 of 14 patients (85%). Hematopoietic stem cell transplantation (HSCT) was performed in 35.7% (5/14) of patients, with a median age of 9 years (range, 7-17 years) among four reported cases. All transplanted patients were alive at the last follow-up, whereas mortality occurred exclusively among non-transplanted patients, including EBV-positive cases. These findings expand the phenotypic and mutational spectrum of CD137 deficiency and highlight the importance of incorporating copy number variant analysis into exome-based diagnostic pipelines when conventional single-nucleotide variant analysis is inconclusive. HSCT remains the only potentially curative treatment, and early molecular diagnosis is essential to enable timely consideration of HSCT and to mitigate life-threatening EBV-driven immunopathology.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":"220 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13180749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147962601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nucleotide-binding oligomerization domain 2-independent colonization by Turicimonas muris induced by high-fat diet protects against dextran sodium sulfate-induced colitis.","authors":"Hajime Honjo, Tomohiro Watanabe, Yasuo Otsuka, Yasuhiro Masuta, Sho Masaki, Ken Kamata, Kosuke Minaga, Seiichi Omura, Ah-Mee Park, Masatoshi Kudo","doi":"10.1093/cei/uxag057","DOIUrl":"10.1093/cei/uxag057","url":null,"abstract":"<p><p>The development of inflammatory bowel diseases is postulated to be driven by the interaction between genetic susceptibility and environmental factors, resulting in proinflammatory cytokine responses to intestinal dysbiosis. Loss-of-function mutations in the nucleotide-binding oligomerization domain 2 gene (NOD2) are the strongest risk factor for Crohn's disease (CD); however, environmental factors affecting CD development have been poorly defined in patients with NOD2 mutations. In this study, we investigated whether high-fat diet (HFD), one of the possible environmental risk factors for CD, acts synergistically with NOD2 deficiency to promote dextran sodium sulfate (DSS)-induced colitis in mice. NOD2-intact (NOD2+/+) and NOD2-deficient (NOD2-/-) mice were challenged with DSS after exposure to normal diet (ND) or HFD. Fecal microbiota composition was determined using next-generation sequencing analyses targeting 16S ribosomal RNA. Fecal microbiota transplantation (FMT) was conducted using microbiota from ND- or HFD-fed NOD2+/+ and NOD2-/- mice as donors. The development of DSS-induced colitis was markedly inhibited by HFD in both NOD2+/+ and NOD2-/- mice, which was accompanied by reduced C-C motif chemokine ligand 2 (CCL2) and tumor necrosis factor (TNF)-a expression levels. The FMT data showed that NOD2-independent colonization by Turicimonas muris induced by HFD suppressed DSS-induced colitis via the downregulation of colonic CCL2 and TNF-a responses. These data suggest that HFD protected against DSS-induced colitis in mice with or without intact NOD2 by promoting colonization by T. muris. Although avoidance of HFD is encouraged in patients with CD, HFD might be useful in the maintenance of intestinal immune homeostasis in experimental colitis.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148954910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evolving understandings for the roles of CD38 protein in autoimmunity and autoimmune disease.","authors":"Xiaochun Ye, Jieying Zhang, Mengping Song, Ping Wang, Irma Ares, Bernardo Lopez-Torres, Marta Martínez, María-Rosa Martínez-Larrañaga, Jorge-Enrique Maximiliano, Arturo Anadón, Xu Wang, María-Aránzazu Martínez","doi":"10.1093/cei/uxag014","DOIUrl":"10.1093/cei/uxag014","url":null,"abstract":"<p><p>Autoimmune diseases are chronic idiopathic disorders characterized by inflammatory responses. Cluster of differentiation 38 (CD38), a surface molecule with enzymatic and signalling capabilities, contributes to the regulation of NAD+ metabolism and mediates various intracellular pathways. Recent research has revealed the influence of the CD38 protein in the pathogenesis of autoimmune diseases. During inflammation, CD38 is involved in regulating biological processes such as cell recruitment, cell activation, cytokine and chemokine release, antigen presentation, and phagocytosis. Dysfunctional CD38 induces autoimmune diseases. CD38 is expressed at low levels in various haematopoietic systems and tissues but exhibits elevated expression in multiple myeloma and plasma cells. CD38-targeted monoclonal antibodies with favourable therapeutic effects have been discovered, such as isatuximab, daratumumab, and mezagitamab. Although CD38-targeted antibodies were originally developed to eliminate malignant immune cells and inhibit their strong activation, these monoclonal antibodies can also inhibit autoantibodies production in autoimmune diseases. CD38 protein is a promising biomarker of autoimmune disease diagnosis and a potential therapeutic target for the treatment of autoimmune diseases. In this review article, we will focus on the latest findings on the involvement of CD38 in autoimmunity and autoimmune disease and assess the value of research and therapeutic application of CD38 in disease control.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13020543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147431144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical, genetic, and functional characterization of novel NFKB1 variants in Chinese patients with primary immunodeficiency.","authors":"Jingyuan Zhang, Huacong Cai, Tienan Zhu, Min Shen","doi":"10.1093/cei/uxag033","DOIUrl":"10.1093/cei/uxag033","url":null,"abstract":"<p><p>The nuclear factor κB (NF-κB)-related disorders encompassed not only common variable immunodeficiency but also manifestations of autoinflammation, autoimmunity, and malignancies. While most cases have been reported in European populations, reports in the Chinese population are sparse. Clinical data and genetic variants from four Chinese patients with NFKB1 variants, alongside four previously reported cases, were analyzed and compared with an international cohort. Additionally, comprehensive in vitro functional assays-including immunoblotting, transcript analyses, dual-luciferase reporter, and co-immunoprecipitation assays-were conducted to explore the molecular defects of the novel variants. Our cohort included three men and one woman, all presenting with recurrent fever and hypogammaglobulinemia. Three patients experienced recurrent sinopulmonary infections, accompanied by decreased B cells and NK cells, while two patients developed pneumonia, bronchiectasis, and hepatitis. Three novel NFKB1 (NM_003998) variants were identified: c.559C > T (p. Arg187Trp), c.1509del (p. Glu504Argfs*19), and c.1753-11_1760del (p. Thr585Alafs*9). Functional analyses revealed distinct pathomechanisms: the frameshift/splicing variants drive classical haploinsufficiency via nonsense-mediated mRNA decay (NMD), triggering compensatory inflammatory hyperactivation; conversely, the p.Arg187Trp missense variant maintains protein stability and heterodimerization but strictly abolishes DNA-binding capacity. Compared to a previously reported cohort, Chinese patients were predominantly male, had a later median age of onset and diagnosis. Notably, Chinese patients exhibited a higher prevalence of hepatitis (25%) and cirrhosis (12.5%), potentially reflecting the high endemicity of hepatitis B virus in China. They also showed increased rates of viral infections, sepsis, and bronchiectasis, with more pronounced reductions in NK and B cells. In contrast, autoimmune diseases and bronchitis were less frequent than in the foreign cohort. This study represents the first and largest case series of Chinese patients with NF-κB1-related diseases, providing molecular characterization for three novel variants. In this limited case series, the observed delayed onset and frequent hepatic complications in our cohort may reflect regional factors, such as HBV endemicity, or ascertainment bias. Our findings underscore that suspected AOSD accompanied by hypogammaglobulinemia warrants immediate genetic investigation. Early diagnosis is essential to prioritize immunoglobulin replacement and prevent fatal complications from immunosuppressive therapy.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13289753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hereditary angioedema: on-demand treatment and long-term prophylaxis-a global reality.","authors":"Cassim Akhoon, Sorena Kiani-Alikhan","doi":"10.1093/cei/uxag043","DOIUrl":"10.1093/cei/uxag043","url":null,"abstract":"<p><p>Hereditary angioedema (HAE) is a rare disorder of recurrent swellings of the subcutaneous and/or mucosal tissues due to defects in the contact system regulation of bradykinin production. The swellings can be disfiguring, cause debilitating abdominal pain, or be fatal with laryngeal obstruction. Over the last decade, there have been immense successes in management of HAE owing to the development of drugs targeting the contact system. This review focuses on management of HAE due to C1-esterase inhibitor (C1-INH) deficiency/dysfunction, including a global perspective which is under-represented in the literature. HAE with normal C1-INH is outside the scope of this article. The review provides summaries of clinical trials that have led to licensing of new HAE medications and discusses access to these modern drugs from a global perspective.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13560080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The 'target tissues' as orchestrators of autoimmune responses: the paradigm of Sjögren's syndrome.","authors":"Maria Filika, Stergios Katsiougiannis","doi":"10.1093/cei/uxaf078","DOIUrl":"10.1093/cei/uxaf078","url":null,"abstract":"<p><p>Systemic autoimmune diseases have been traditionally studied with a special focus on the immune system and less attention was paid to the roles of target tissues that are being exposed to the immune assault. For many common autoimmune diseases accumulating data unravel and highlight the potential role of the target tissues as orchestrators of the autoimmune responses. In this selective review, using Sjögren's disease (SjD) as a paradigm, we discuss the role of salivary gland epithelial cells (SGEC) not as innocent bystander targets of autoimmune responses, but rather as initiators and amplifiers of the inflammatory reactions. In fact, SGEC patients with Sjögren's disease are characterized by a unique phenotype which is capable of initiating and perpetuating both innate and adaptive immune responses in the glandular microenvironment. Aberrant expression and function of TLRs and IFN pathways, lymphocyte activating proteins as well as rewired cellular metabolism and antigen-presenting features, shape this distinct auto-antigenic phenotype of SGEC. These discoveries and ideas regarding the regulatory potential of the target SGEC in Sjögren's disease add a new dimension to our concept of regulatory circuits in autoimmunity.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145767213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PSMB8 stratifies therapy response in eosinophilic esophagitis.","authors":"Xinyi Wei, Sabrina Degen, Theresa Hironimus, Tobias Rechenauer, Katharina Yankouskaya, Aline Rückel, Margit Schmid, Daniel Rieger, Christoph Ehrsam, Adrian P Regensburger, Alexander Schnell, Anja Rabe, Anjona Schmidt-Choudhury, Andrea Tannapfel, Jan De Laffolie, Stefan Schumann, Tobias Schwerd, Hannes Hoelz, Ida Allabauer, Pooja Gupta, Wolfgang Krebs, Arndt Hartmann, Joachim Woelfle, Ralf Rieker, Andre Hoerning","doi":"10.1093/cei/uxag012","DOIUrl":"10.1093/cei/uxag012","url":null,"abstract":"<p><p>Proton pump inhibitors (PPIs) are an effective first-line treatment for eosinophilic esophagitis (EoE). However, half of the patients are refractory to PPI therapy, and predictive markers for therapy decision are lacking. Thus, this study aimed to investigate the differences in esophageal immunologic transcriptome between PPI-non-responders and PPI-responders and identify molecular biomarkers to guide therapy decisions. Forty-eight pediatric EoE patients were enrolled and classified due to PPI-therapy response. Pre-treatment esophagus biopsy was collected for gene expression analysis, differentially expressed genes (DEGs) between PPI-responders and non-responders were identified, followed by gene enrichment and protein-protein interaction network analyses. Expression of identified hub genes was confirmed by immunohistochemistry in an extended cohort comprising 62 patients. PPI-non-responders and responders exhibit a partially different transcriptomic profile, as 12 DEGs were up-regulated and one down-regulated. These DEGs are closely related to antigen processing and presentation function. PSMB8 was identified as a hub gene differing between these two groups, and immunohistochemistry confirmed significantly increased expression in PPI-non-responders (P < 0.0001). Notably, receiver operating characteristic curves curve analysis of PSMB8 reveals it as highly predictive for PPI response (sensitivity/specificity: 0.61/1.00). PPI-non-responding EoE patients exhibited a more profound dysregulation of gene expression. PSMB8 represents a promising esophageal biomarker for predicting therapy response in pediatric EoE.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":"220 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13062531/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147638177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: CD137 deficiency patients: two new patients and review of the literature.","authors":"","doi":"10.1093/cei/uxag058","DOIUrl":"10.1093/cei/uxag058","url":null,"abstract":"","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":"220 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13623001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management of hereditary angioedema in the UK: a comparison with international guidelines.","authors":"Patrick F K Yong, Jolanta Bernatoniene, Rachel Annals, Charu Chopra, Tanya Coulter, Sarah Denman, Anthony Dorr, Tariq El-Shanawany, Alexandros Grammatikos, Padmalal Gurugama, Rashmi Jain, Sorena Kiani-Alikhan, Lucy Leeman, Lorena Lorenzo, Ania Manson, Sadia Noorani, Smita Patel, Arthur Price, Ravi Sargur, Cathal Steele, Catherine Stroud, Cassim Akhoon, Ariharan Anantharachagan, Emily Carne, Samuel Chee, Joanne Miller, Stephen Owens, Christine Symons, Ky-Lyn Tan, Michael D Tarzi, Scott Hackett, Angela Metcalfe, Sinisa Savic, Tomaz Garcez","doi":"10.1093/cei/uxag056","DOIUrl":"10.1093/cei/uxag056","url":null,"abstract":"<p><p>Hereditary angioedema (HAE) is a rare genetic disorder characterized by recurrent episodes of swelling, which can potentially be life-threatening, resulting in substantial physical, psychological, educational, and occupational burden. Treatment of HAE is divided into on-demand treatment for acute attacks and long-term prophylaxis for prevention of attacks, and there are now several effective therapies available. However, in the UK, use of on-demand therapy is intended for attacks defined as clinically significant, and access to long-term prophylaxis is determined primarily by frequency-based criteria. In this policy-focused review, we compare UK access criteria with international guidelines on best practice. We conclude that UK access criteria result in a group of HAE patients with persisting unmet need, and this may have a greater impact in children and young people. In view of this, we recommend greater flexibility in access criteria, allowing clinical judgement, shared decision-making, and broader measures of disease burden to inform treatment eligibility, so we can individualize care and fully meet the needs of these patients.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-33 blockade attenuates vascular inflammation in a mouse model of Kawasaki disease vasculitis.","authors":"Thacyana T Carvalho, Benjamin L Ross, Prasant K Jena, Asli E Atici, Angela C Gomez, Michael C Fishbein, Emily A Aubuchon, Youngho Lee, Richard T Lee, Elizabeth A Jacobsen, Waldiceu A Verri, Shuang Chen, Timothy R Crother, Moshe Arditi, Magali Noval Rivas","doi":"10.1093/cei/uxaf086","DOIUrl":"10.1093/cei/uxaf086","url":null,"abstract":"<p><p>The immune mechanisms underlying Kawasaki disease (KD), a febrile systemic vasculitis in children, are poorly understood. Reports indicate elevated levels of circulating IL-33 in acute KD patients; however, if IL-33 contributes to the pathogenesis of KD vasculitis remains unclear. Here, we used the Lactobacillus casei cell wall extract (LCWE)-induced murine model of KD to determine the contribution of IL-33 to vasculitis development. We observed increased expression of Il33 transcripts and IL-33 protein in LCWE-induced cardiovascular lesions. Bone marrow chimera experiments suggest that IL-33 production by both hematopoietic and stromal cells is important for LCWE-induced KD vasculitis; however, single-cell RNA sequencing, spatial transcriptomics, and flow cytometric analysis revealed that stromal cells were the predominant sources of IL-33. Furthermore, immune cells infiltrating LCWE-induced cardiovascular lesions expressed Il1rl1 transcripts, coding for the IL-33 receptor ST2. In vitro stimulation of bone marrow-derived macrophages with IL-33 enhanced their production of IL-1b and TNF-α. In vivo blockade of IL-33, using either neutralizing IL-33 antibody or Il33-/- mice, effectively attenuated LCWE-induced cardiovascular inflammation. Our results indicate that IL-33 contributes to LCWE-induced vascular inflammation through redundant mechanisms across multiple immune cell subsets rather than a single population and highlight IL-33 as a potential therapeutic target.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":"220 1","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12803022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}