Immunology最新文献

{"title":"Optimization of Immunotherapy Strategies Based on Spatiotemporal Heterogeneity of Tumour-Associated Tissue-Resident Memory T Cells","authors":"Yile Shang,&nbsp;Yinjun He,&nbsp;Xiang Zhang,&nbsp;Wenguang He,&nbsp;Hanju Hua,&nbsp;Feng Ye,&nbsp;Xile Zhou,&nbsp;Yandong Li,&nbsp;Weixiang Zhong,&nbsp;Guosheng Wu,&nbsp;Weiqin Jiang","doi":"10.1111/imm.13924","DOIUrl":"10.1111/imm.13924","url":null,"abstract":"<p>Tissue-resident memory T cells (TRMs) reside in peripheral tissues and provide rapid immune defence against local infection and tumours. Tumour-associated TRMs share common tissue-resident features and formation mechanisms, representing some unique subsets of tumour-infiltrating lymphocytes (TILs). However, differences in the tumour microenvironment(TME) and tumour evolution stage result in TRMs exhibiting temporal and spatial heterogeneity of phenotype and function not only at different stages, before and after treatment, but also between tumours originating from different tissues, primary and metastatic cancer, and tumour and adjacent normal tissue. The infiltration of TRMs is often associated with immunotherapy response and favourable prognosis; however, due to different definitions, it has been shown that some subtypes of TRMs can also have a negative impact. Therefore, it is crucial to precisely characterise the TRM subpopulations that can influence the therapeutic efficacy and clinical prognosis of various solid tumours. Here, we review the spatiotemporal heterogeneity of tumour-associated TRMs, as well as the differences in their impact on clinical outcomes. We also explore the relationship between TRMs and immune checkpoint blockade (ICB) and TIL therapy, providing insights into potential new targets and strategies for immunotherapy.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"123-133"},"PeriodicalIF":4.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13924","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669808","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":"Reversing Microglial Polarisation by High Intensity Interval Training: A Novel Approach to Mitigate Inflammatory Responses in Osteoarthritis via Jak2/Stat3 Pathway","authors":"Xinwei Wang,&nbsp;Mingxia Gao,&nbsp;Peng Xia,&nbsp;Ziqi Ye,&nbsp;Fanghui Li,&nbsp;Xueping Li","doi":"10.1111/imm.13921","DOIUrl":"10.1111/imm.13921","url":null,"abstract":"<p>Osteoarthritis (OA) is associated with inflammatory responses linked to microglial polarisation within the central nervous system. However, exploring therapeutic approaches and their underlying mechanisms remains a direction for future research. The present study investigates the potential of high-intensity interval training (HIIT) to alleviate inflammation and facilitate the shift from M1 to M2 microglial polarisation via the Jak2/Stat3 pathway in an OA rat model. Wistar rats were induced with OA via intra-articular injection of monosodium iodoacetate and subsequently underwent HIIT for six consecutive weeks after a 4-week establishment period. Pain thresholds were measured using the von Frey test. Immunofluorescence detected Tmem119, SP, Glu, c-Fos, and IL-6, while flow cytometry analysed CD68 and CD163 levels. Proteomics compared the protein differences between the OA and HIIT groups. The Jak2/Stat3 pathway was activated in OA rats with C-A1 injections, followed by HIIT and subsequent Western blot analysis of inflammatory cytokines. The results indicated a significant decrease in pain threshold from the third to the tenth week in OA rats, while HIIT was found to increase pain thresholds. HIIT was found to promote M1 to M2 microglial polarisation and downregulate the expression of Tmem119, SP, Glu, c-Fos, and IL-6. Additionally, HIIT was more effective in suppressing Jak2 and Stat3 expression levels compared to OA rats. Activation of the Jak2/Stat3 pathway significantly increased the expression of Glu, c-fos, SP, and IL-6, but HIIT reversed these OA-induced increases. Compared to the OA + C-A1 group, the expression levels of Glu, c-fos, SP, and IL-6 were significantly reduced in the OA + C-A1 + HIIT group. In conclusion, HIIT effectively mitigates OA-induced inflammatory responses by reversing microglial polarisation through the Jak2/Stat3 pathway.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"240-250"},"PeriodicalIF":4.9,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13921","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633932","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":"Deciphering the IgG Idiotype Network Through Proteomic Analysis of Potential Targets in SARS-CoV-2-Induced Immune Responses","authors":"Nicolle Rakanidis Machado,&nbsp;Beatriz Oliveira Fagundes,&nbsp;Lais Alves do Nascimento,&nbsp;Isabella Siuffi Bergamasco,&nbsp;Fabio da Ressureição Sgnotto,&nbsp;Iara Grigoletto Fernandes,&nbsp;Juliana Ruiz Fernandes,&nbsp;Thalyta Nery Carvalho Pinto,&nbsp;João Vitor Silva da Borges,&nbsp;Gil Benard,&nbsp;Maria Notomi Sato,&nbsp;Jefferson Russo Victor","doi":"10.1111/imm.13919","DOIUrl":"10.1111/imm.13919","url":null,"abstract":"<div>\u0000 \u0000 <p>The association between COVID-19 and autoimmune diseases has gained increasing recognition, yet the specific targets of SARS-CoV-2-induced IgG are currently in focus for several studies. This study aims to explore the proteomic targets of these antibodies and their potential role in autoimmunity. We utilised a human proteome microarray encompassing 23 736 unique proteins, including isoform variants and fragments, as catalogued by the Human Protein Atlas. Serum samples were analysed from four groups: healthy controls (N-exp HC), individuals vaccinated with protein-based vaccines (N-Cov Vac) and patients with moderate or severe COVID-19 (COVID-Mod and COVID-Sev). The evaluation of SARS-CoV-2-induced IgG antibodies revealed their potential to recognise multiple human proteins. Key targets included interferon alpha (IFN-α), tumour growth factor beta (TGF-β), interleukin 1 (IL-1), CXCL16, TGF-β receptors, CD34, CD47 and BCL2. The antibodies also targeted proteins from genes overexpressed in various immune cells, such as CD4+ and CD8+ T cells, γδ T cells, B cells, dendritic cells and NK cells. Reactivity was also observed with proteins specifically expressed in multiple organs, including the brain, liver, lungs and heart. Targeting patterns differed between COVID-19 patients and controls, with some proteins showing differential recognition in moderate versus severe cases. Furthermore, we evaluated the protein–protein interaction network (PPIN) of all targeted proteins and observed minimal structural homology and co-expression among the evaluated proteins, with almost no relation to the SARS-CoV-2 immune system reactome. The results suggest that the profile of SARS-CoV-2-induced IgG autoantibodies is associated with disease severity. In contrast, protein-vaccinated individuals exhibited a profile similar to non-exposed controls, suggesting that autoreactive IgG is specifically linked to active SARS-CoV-2 infection. These findings reveal a complex network of SARS-CoV-2-induced IgG idiotypes capable of targeting human proteins, not merely through simple cross-recognition of homologous proteins. This highlights the need for further investigations to determine whether they may influence COVID-19 pathophysiology and its clinical outcomes.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"226-239"},"PeriodicalIF":4.9,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Augmenting Macrophages Apoptosis Induced by Carnitine Palmitoyl Transferase 1A Inhibition via Acetyl-CoA-Associated Protein Acetylation","authors":"Guochao Shi,&nbsp;Rong Wang,&nbsp;Chunrong Huang","doi":"10.1111/imm.13917","DOIUrl":"10.1111/imm.13917","url":null,"abstract":"<div>\u0000 \u0000 <p>Macrophage apoptosis contributes to acute lung injury (ALI). However, the relationship between cell metabolism and the apoptosis of macrophages remains unclear. In our study, murine alveolar macrophages (MH-S) were stimulated by lipopolysaccharide (LPS) to induce an apoptosis model; cell viability, mitochondrial membrane potential (MMP) and apoptosis rate were determined. TCA metabolites and fatty acids were measured; qPCR and western blot were used to detect gene and protein expressions. The LPS-induced ALI mice model was established, and pathological changes, inflammatory cytokines, and protein acetylation were evaluated. The results showed that LPS exposure impaired cell viability and increased apoptosis of alveolar macrophages (AM) in a concentration-dependent manner. LPS also downregulated the expression of the FAO rate-limiting enzyme carnitine palmitoyl transferase 1A (CPT1A), which was accompanied by suppression of fatty acid oxidation (FAO) and alterations of the fatty acid profile. CPT1A inhibitor etomoxir also promoted cell apoptosis of AM and decreased MMP. Overexpression of CPT1A ameliorated cell apoptosis of AM induced by LPS. Etomoxir and LPS decreased acetyl-CoA levels, and supplementation of acetyl-CoA prevented LPS-induced cell apoptosis. In addition, LPS led to the alteration of acetylated protein profiles. In vivo study, excessive cell apoptosis, decreased expression of proteins related to FAO, and decreased acetyl-CoA levels were detected in ALI animal models. Acetyl-CoA could relieve the apoptosis and inflammation in the lung induced by LPS. These findings suggested the essential role of CPT1A and acetyl-CoA in cell apoptosis of AM induced by LPS.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"214-225"},"PeriodicalIF":4.9,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endogenous ERMAP Affects T-Cell Function in EAE Mice","authors":"Keke He,&nbsp;Kezhu Chen,&nbsp;Rong Hu,&nbsp;Tinghao Wen,&nbsp;Yuandi Li,&nbsp;Lu Xia,&nbsp;Li Xiao,&nbsp;Youbo Zhao,&nbsp;Dongbing Cui,&nbsp;Jie Gao,&nbsp;Lu Liu,&nbsp;Laijun Lai,&nbsp;Min Su","doi":"10.1111/imm.13910","DOIUrl":"10.1111/imm.13910","url":null,"abstract":"<div>\u0000 \u0000 <p>Multiple sclerosis (MS) is a central nervous system (CNS) autoimmune disease (AID) mediated by myelin-reactive CD4⁺ T cells. Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model of human MS. Erythrocyte membrane-associated protein (ERMAP) is a novel erythrocyte-specific adhesion/receptor molecule associated with erythrocyte adhesion. We have previously characterised it as a novel inhibitory immune checkpoint molecule and demonstrated that recombinant ERMAP proteins ameliorate EAE; however, the specific mechanism of action of ERMAP and the effects of endogenous ERMAP on T-cell function are largely unknown. In this study, we investigate the role of endogenous ERMAP in T-cell and macrophage homeostasis and EAE development. We show here that erythrocyte membrane-associated protein (ERMAP) gene knockout (ERMAP^−/−) mice have increased numbers of T cells and pro-inflammatory M1 macrophages and enhanced T-cell activation, as compared to wild-type (ERMAP^+/+) mice. When induced to develop EAE, ERMAP^−/− mice have more severe EAE symptoms and pathology, which are related to increased numbers of T cells (especially Th1 and Th17 T cells) and M1 macrophages, enhanced activation of T cells, and increased generation of inflammatory cytokines, but decreased proportion of Th2 T cells, regulatory T cells (Tregs), and anti-inflammatory M2 macrophages. Global gene analysis by RNA-seq shows that signalling molecules in the peroxisome proliferator-activated receptor (PPAR) pathway are decreased in ERMAP^−/− mice. Our results suggest that endogenous ERMAP plays an important role in T-cell and macrophage homeostasis and EAE development.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"200-213"},"PeriodicalIF":4.9,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Original Antigenic Sin in CD4+ T Cells","authors":"Mingran Zhang,&nbsp;Junling Ma,&nbsp;Meili Li","doi":"10.1111/imm.13916","DOIUrl":"10.1111/imm.13916","url":null,"abstract":"<div>\u0000 \u0000 <p>Original antigenic sin (OAS) describes the phenomenon in which prior exposure to an antigen weakens the adaptive antibody response to a subsequent heterologous infection. This phenomenon can diminish the effectiveness of immunity acquired through vaccination or previous infections. We demonstrate that OAS arises because CD4+ T cell proliferation and regulation signals are antigen-nonspecific. Rapidly responding memory CD4+ T cells trigger regulatory T cell (Tregs) responses, which prematurely suppress the naïve CD4+ T cell response, leading to a similar OAS effect in CD4+ T cells. This mechanism is illustrated through a mathematical model incorporating naïve and memory CD4+ T cell proliferation, interleukin-2 (IL-2), and Tregs. The model, calibrated with experimental data, employs numerical simulations to analyse how CD4+ T cell responses vary with the degree of cross-reactivity between memory CD4+ T cells and the antigen associated with the secondary infection. The findings indicate that the immune response is weakest at an intermediate level of cross-reactivity, a key characteristic of OAS. This mechanism may also explain OAS in antibody responses.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"165-179"},"PeriodicalIF":4.9,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computer Integrated Dominant Epitopes Evoke Protective Immune Response Against Streptococcus pneumoniae","authors":"Hitesh Harsukhbhai Chandpa,&nbsp;Shovan Naskar,&nbsp;Jairam Meena","doi":"10.1111/imm.13920","DOIUrl":"10.1111/imm.13920","url":null,"abstract":"<div>\u0000 \u0000 <p><i>Streptococcus pneumoniae</i> is a gram-positive bacterium responsible for various diseases like pneumonia, acute otitis media, sinusitis, meningitis and bacteraemia. These diseases cause a significant amount of morbidity and mortality. Although polysaccharide vaccines are available, the protection provided by these vaccines is serotype-dependent and not enough in sensitive populations like children and older people. Designing a subunit vaccine by using proteins that are responsible for the pathogenesis of diseases can provide better protection against bacterial infections. In this study, we present the design of a novel multi-epitope vaccine against <i>Streptococcus pneumoniae</i> using an immunoinformatic approach. More than 1170 epitopes were identified against B cells, cytotoxic T lymphocytes and helper T lymphocytes from more than 60 pneumococcal proteins. Epitopes were further screened, and potential epitopes were selected for vaccine development. Seven different vaccine combinations that harbour the 15 dominant B-cell, cytotoxic T cell and helper T cell epitopes were evaluated with linker and β-defensin adjuvant to finalise the best vaccine construct. Bioinformatics tools were used to analyse the construct's physicochemical properties, secondary and tertiary structures, allergenicity, antigenicity and immunogenicity. Docking studies with the TLR-4 receptor and molecular dynamics simulations indicated strong binding affinity and stability. In silico immune response simulations predicted robust IgG immune response generation and observed more than 200 000 IgG₁ + IgG₂ counts per mL. Similarly, cell-mediated immunity was also enhanced by the designed vaccine construct. The construct was codon-optimised and cloned in silico for expression in <i>Escherichia coli</i>. These findings suggest that the construct is a promising candidate for further experimental validation.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"180-199"},"PeriodicalIF":4.9,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytotoxic Signature and IFN-γ Production Dominate CD4+ T-Cell Response During Human Toxoplasmosis","authors":"Priscilla Miranda Henriques,&nbsp;Gregório Guilherme Almeida,&nbsp;Inga Rimkute,&nbsp;Luara Isabela dos Santos,&nbsp;Thomas Liechti,&nbsp;Ana Paula Marino,&nbsp;Isabela Natália Pascoal Campos do Vale,&nbsp;Daniel Vitor Vasconcelos-Santos,&nbsp;Olindo Assis Martins-Filho,&nbsp;Ricardo Tostes Gazzinelli,&nbsp;Mario Roederer,&nbsp;Alan Sher,&nbsp;Andréa Teixeira-Carvalho,&nbsp;Dragana Jankovic,&nbsp;Lis Ribeiro do Valle Antonelli","doi":"10.1111/imm.13912","DOIUrl":"10.1111/imm.13912","url":null,"abstract":"<p><i>Toxoplasma gondii</i> is a highly versatile parasite that infects most warm-blooded animals and is a major cause of retinochoroiditis and uveitis in humans. The pathophysiology of these conditions remains poorly understood. Both parasite virulence and host inflammatory response contribute to the development of ocular disease. While CD4⁺ T cells play a critical role in host resistance to <i>Toxoplasma</i> infection, their kinetics and effector functions, as well as their contribution to the clinical outcome of the infection, including ocular involvement, remain poorly understood. To address this question, we investigated the immune response during acute and convalescent toxoplasmosis and stratified patients further based on the presence or absence of ocular disease. We found that <i>T. gondii</i> infection leads to decreased and increased proportions of central and effector memory CD4⁺ T cells, respectively. Applying unsupervised analysis, distinct CD4⁺ T-cell subsets were determined. Among 50 clusters, 10 produced cytotoxic proteins (granzyme B and perforin) and one produced cytokines upon antigen-specific stimulation. We observed that proportions of five CD4⁺ T-cell clusters out of 50 were different during acute disease between <i>T. gondii</i>-infected patients with and without ocular lesions. Interestingly, three of the five displayed a cytotoxic signature indicating their possible involvement in ocular immunopathology. Taken together, our results reveal that during <i>T. gondii</i> infection, CD4⁺ T cells not only develop a Th1 cytokine profile, but also acquire previously unappreciated cytotoxic capacity/function. These results, while underscoring the complexity of the CD4⁺ T-cell response to <i>T. gondii</i>, suggest that specific subsets may be involved in the development of pathology and provide possible targets for therapeutic intervention.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"151-164"},"PeriodicalIF":4.9,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13912","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143541260","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":"Ammonia-Induced Cell Death: A Novel Frontier to Enhance Cancer Immunotherapy","authors":"Urushi Rehman,&nbsp;Garima Gupta,&nbsp;Amirhossein Sahebkar,&nbsp;Prashant Kesharwani","doi":"10.1111/imm.13918","DOIUrl":"10.1111/imm.13918","url":null,"abstract":"<p>Cancer immunotherapy has revolutionized treatment paradigms, but its efficacy is often curtailed by T-cell exhaustion and the suppressive tumour microenvironment. Recent studies reveal a novel mechanism of T-cell demise termed ammonia-induced cell death (AICD), which significantly impacts effector CD8+ T-cell survival and function. This phenomenon arises from metabolic reprogramming during immune activation, wherein heightened glutamine metabolism leads to the accumulation of toxic ammonia levels. Ammonia damages lysosomes and mitochondria, disrupting cell balance and causing apoptosis. These insights provide a unique metabolic perspective on T-cell attrition, underscoring the critical interplay between metabolic byproducts and immune regulation. Targeting AICD offers promising therapeutic avenues to bolster immunotherapy. Strategies such as inhibiting ammonia transport, enhancing autophagic pathways and employing ammonia scavengers may extend T-cell longevity and improve antitumor efficacy. Moreover, integrating ammonia modulation with established immunotherapies, including immune checkpoint inhibitors and chimeric antigen receptor (CAR) T-cell therapy, could yield synergistic benefits. Addressing this metabolic bottleneck is particularly compelling in immune ‘cold’ tumours resistant to conventional therapies. However, further research is essential to refine these interventions, evaluate safety profiles and explore broader applications across cancer types. Ammonia metabolism thus represents a transformative frontier in advancing cancer immunotherapy and precision oncology.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 1","pages":"16-20"},"PeriodicalIF":4.9,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13918","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143541114","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":"Successful Treatment of Chronic Rhinosinusitis With Nasal Polyps (CRSwNP) With Tezepelumab: A Case Report.","authors":"Mattia Cristallo, Mirco Filieri, Federico Spataro, Loredana Muolo, Eustachio Nettis, Attilio Di Girolamo","doi":"10.1111/imm.13915","DOIUrl":"https://doi.org/10.1111/imm.13915","url":null,"abstract":"","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}