Clinical and experimental immunology最新文献

{"title":"Neuro-Behçet's disease: an update of clinical diagnosis, biomarkers, and immunopathogenesis.","authors":"Haoting Zhan, Linlin Cheng, Yongzhe Li","doi":"10.1093/cei/uxae123","DOIUrl":"10.1093/cei/uxae123","url":null,"abstract":"<p><p>Neuro-Behçet's disease (NBD) is a more severe but rare symptom of Behçet's disease, which is mainly divided into parenchymal NBD (p-NBD) involving brain stem, spinal cord, and cerebral cortex. Non-p-NBD manifests as intracranial aneurysm, cerebral venous thrombosis, peripheral nervous system injuries, and mixed parenchymal and non-parenchymal disease. p-NBD is pathologically characterized by perivasculitis presenting with cerebrospinal fluid (CSF) pleocytosis, elevated total protein, and central nervous system (CNS) infiltration of macrophages and neutrophils, which are subdivided into acute and chronic progressive stages according to relapsing-remitting courses and responses to steroids. The diagnosis of NBD depends heavily on clinical features and magnetic resonance imaging (MRI) findings. The lack of laboratory biomarkers has hindered standard diagnostics. CSF interleukin (IL)-6 is the most investigated dimension of NBD and correlates with NBD activity, therapeutic responses, and prognosis. Further investigations have focused on inflammatory biomarkers that reflect the activation of innate and adaptive immune responses. Higher levels of CSF migration inhibitory factor and immunosuppressive acidic protein indicated the activation of macrophages in the CNS; increased IL-17, IL-10, T-bet/GATA-3, and retinoic acid related orphan receptor (ROR)-γt/Foxp3 ratios, marking the disrupted scale of the Th1/Th2 and Th17/Treg axis; and elevated B-cell activating factor of the TNF family (BAFF) and IgA/IgM intrathecal synthesis, suggesting that B cells play a dominant role in NBD. CNS destruction and degeneration as a consequence of neuroinflammatory cascades were confirmed by elevated CSF levels of NFL, β2MG, and MBP. Autoantibodies, including anti-STIP-1, anti-Mtch1, anti-B-Crystallin, and anti-m-Hsp65, provide substantial evidence for autoimmune essence and underlying microbiological infections in NBD immunopathogenesis. We summarized opinions on the clinical diagnosis, biomarkers, and pathological findings of NBD.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945582","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":"Senescence-related genes are associated with the immunopathology signature of American tegumentary leishmaniasis lesions and may predict progression to mucosal leishmaniasis.","authors":"Carlos Henrique Fantecelle, Luciana Polaco Covre, Paola Oliveira Lopes, Isabela Valim Sarmento, Debora Decote-Ricardo, Célio Geraldo Freire-de-Lima, Herbert Leonel de Matos Guedes, Maria Inês Fernandes Pimentel, Fatima Conceição-Silva, Ana C Maretti-Mira, Valéria M Borges, Lucas Pedreira de Carvalho, Edgar Marcelino de Carvalho, David Mosser, Aloisio Falqueto, Arne N Akbar, Daniel Claudio Oliveira Gomes","doi":"10.1093/cei/uxae088","DOIUrl":"10.1093/cei/uxae088","url":null,"abstract":"<p><p>The American tegumentary leishmaniasis (ATL) is caused by protozoans of the genus Leishmania and varies from mild localized cutaneous leishmaniasis (LCL) form to more severe manifestations such as the diffuse cutaneous leishmaniasis (DCL) form and the mucosal leishmaniasis (ML) form. Previously, we demonstrated the accumulation of senescent cells in skin lesions of patients with LCL. Moreover, lesional transcriptomic analyses revealed a robust co-induction of senescence and pro-inflammatory gene signatures, highlighting the critical role of senescent T cells in orchestrating pathology. In this work we hypothesized that senescent cells might operate differently among the ATL spectrum, potentially influencing immunopathological mechanisms and clinical outcome. We analysed previously published RNA-Seq datasets of skin biopsies of healthy subjects and lesional skin from DCL patients, LCL patients, and LCL patients that, after treatment, progressed to mucosal leishmaniasis (MLP). Our findings demonstrate a robust presence of a CD8 T-cell signature associated with both LCL and MLP lesions. Moreover, both inflammatory and cytotoxic signatures were significantly upregulated, showing a strong increase in MLP and LCL groups, but not DCL. The senescence signature was elevated between LCL and MLP groups, representing the only distinguishable signature of immunopathology between them. Interestingly, our analyses further revealed the senescence signature's capacity to predict progression from LCL to mucosal forms, which was not observed with other signatures. Both the senescence-signature score and specific senescence-associated genes demonstrated an increased capacity to predict mucosal progression, with correct predictions exceeding 97% of cases. Collectively, our findings contribute to a comprehensive understanding of immunosenescence in ATL and suggest that senescence may represent the latest and most important signature of the immunopathogenisis. This highlights its potential value in predicting disease severity.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459410","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":"Increased expression of CXCL10 and CCL3 salivary gland chemokines in primary Sjögren's syndrome detected and systematically quantified using RNAscope®in situ hybridization.","authors":"Hanne Borge, Ingrid Beate Ringstad, Lara A Aqrawi, Siren Fromreide, Harsh Nitin Dongre, Hilde Kanli Galtung, Janicke Liaaen Jensen, Kathrine Skarstein","doi":"10.1093/cei/uxae087","DOIUrl":"10.1093/cei/uxae087","url":null,"abstract":"<p><p>Primary Sjögren's syndrome is a chronic inflammatory disease characterized by the destruction of exocrine glands. We have previously shown significantly upregulated levels of CXCL10 and CCL3 chemokines in saliva from Sjögren's syndrome patients. In this study, we examined the expression pattern and localization of these chemokines at the site of inflammation in patients' minor salivary glands using novel RNAscope® in situ hybridization. Minor salivary glands from 33 primary Sjögren's syndrome patients and 22 non-Sjögren's syndrome (non-SS) sicca controls were included. The biopsies were formalin-fixed, paraffin-embedded, and histopathologically evaluated. The CXCL10 and CCL3 mRNA expression in the glandular tissue was investigated using reverse transcription quantitative real-time polymerase chain reaction followed by an RNAscope® in situ hybridization. The mRNA expression of CXCL10 was higher than CCL3 in all patients. Significantly elevated expression of CXCL10 and CCL3 was detected in patients that also expressed autoantibody positivity and a positive biopsy for mononuclear cell infiltrates when compared with non-SS sicca controls. CXCL10 was localized as clusters within focal infiltrates as well as adjacent to acinar and ductal epithelium, while CCL3 was expressed as scattered single mRNA molecules in focal infiltrates and in acinar cells. Our findings suggest CXCL10 as a possible disease biomarker in primary Sjögren's syndrome due to its upregulated expression in both saliva and minor salivary glands of patients and the localization in the tissue. This should be re-assessed in a larger primary Sjögren's syndrome patient cohort, followed by additional functional studies to further validate its potential as a disease biomarker.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11771196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142496171","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 B-cells paradigm in systemic sclerosis: an update on pathophysiology and B-cell-targeted therapies.","authors":"Cristina Scaletti, Sara Pratesi, Silvia Bellando Randone, Linda Di Pietro, Corrado Campochiaro, Francesco Annunziato, Marco Matucci Cerinic","doi":"10.1093/cei/uxae098","DOIUrl":"10.1093/cei/uxae098","url":null,"abstract":"<p><p>Systemic sclerosis (SSc) is considered a rare autoimmune disease in which there are alterations of both the innate and adaptive immune response resulting in the production of autoantibodies. Abnormalities of the immune system compromise the normal function of blood vessels leading to a vasculopathy manifested by Raynaud's phenomenon, an early sign of SSc . As a consequence of this reactive picture, the disease can evolve leading to tissue fibrosis. Several SSc-specific autoantibodies are currently known and are associated with specific clinical manifestations and prognosis. Although the pathogenetic role of these autoantibodies is still unclear, their production by B cells and plasma cells suggests the importance of these cells in the development of SSc. This review narratively examines B-cell dysfunctions and their role in the pathogenesis of SSc and discusses B-cell-targeted therapies currently used or potentially useful for the management of end-organ complications.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582148","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 to: Altered expression of caspases-4 and -5 during inflammatory bowel disease and colorectal cancer: Diagnostic and therapeutic potential.","authors":"","doi":"10.1093/cei/uxae103","DOIUrl":"10.1093/cei/uxae103","url":null,"abstract":"","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750123","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":"Docosahexaenoic acid mitigates experimental autoimmune prostatitis by inhibiting Th17 cell differentiation via the PPARγ/NF-κB/IL-17A pathway.","authors":"Weikang Wu, Shaoyu Yue, Xu Wang, WeiYi Li, Lingfan Xu, Yu Guan, Chao-Zhao Liang","doi":"10.1093/cei/uxaf055","DOIUrl":"10.1093/cei/uxaf055","url":null,"abstract":"<p><p>Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a prevalent urological disorder characterized by urinary symptoms, pelvic pain, and sexual dysfunction. The potential inhibitory effects of docosahexaenoic acid (DHA) in relation to dietary consumption on autoimmune disorders have been acknowledged. Nevertheless, the effect of consuming DHA on CP/CPPS is still uncertain. Therefore, we established an experimental autoimmune prostatitis (EAP) model, which is frequently employed in CP/CPPS research. This study aimed to investigate the effects of dietary docosahexaenoic acid (DHA) intake on EAP and to elucidate the underlying mechanisms involved. During the establishment of EAP, non-obese diabetic (NOD) mice were administered either DHA-enriched water or conventional water. The severity of EAP and the Th17 cell responses were evaluated. Furthermore, we investigated the impact of the PPARγ inhibitor GW9662 and the NF-κB activator PMA on mice with EAP that were administered DHA. The findings demonstrated that consumption of DHA reduced the severity of EAP and inhibited the production of Th17 cells. DHA was found to hinder the development of Th17 cells through the PPARγ/NF-κB/IL-17A pathway, as demonstrated by in vitro assays. The administration of GW9662 and PMA resulted in an increase in Th17 cell production, worsening the symptoms of EAP alleviated by the consumption of DHA. The present study revealed that the consumption of DHA mitigates EAP by stimulating the PPARγ/NF-κB/IL-17A pathway, thereby influencing the process of Th17 cell differentiation. The results provide a valuable understanding of the molecular pathways that contribute to the beneficial impacts of dietary variables, including DHA, on CP/CPPS.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12411758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144944943","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":"Expanded senescent CD8 T cells in IMID patients are associated with distinct inflammatory cytokines.","authors":"Marie Naigeon, Samuel Bitoun, Matthieu Roulleaux Dugage, Caroline de Oliveira, Caroline Berthot, Benjamin Besse, Aurélien Marabelle, François-Xavier Danlos, Xavier Mariette, Nathalie Chaput, Gaetane Nocturne","doi":"10.1093/cei/uxaf050","DOIUrl":"10.1093/cei/uxaf050","url":null,"abstract":"<p><p>Using flow cytometry, we assessed circulating T4sen and T8sen proportions at baseline and 3 months after initiating anti-TNF treatment in RA and SpA patients using flow cytometry. Circulating levels of cytokines were measured at baseline. These parameters were associated with demographic variables and disease activity. T4sen and T8sen were compared between RA, SpA, SjD, healthy donors, and cancer patients. T8sen, but not T4sen, accumulated more in patients with IMIDs than in patients with lung cancer and healthy donors. CMV-seropositivity was associated with the accumulation of T8sen. T8sen were associated with high IL-6 in SpA patients and high IP-10 in SjD patients. Anti-TNF did not impact the T8sen proportion of RA and SpA patients. There was a trend toward an increase in T8sen in anti-TNF nonresponders after 3 months of treatment. Senescent CD8 T cells are enriched in IMID patients, suggesting that immune aging is a shared feature of chronic inflammatory diseases. The association between T8sen and distinct inflammatory cytokines underscores the potential role of senescence in shaping immune responses in IMIDs.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12451446/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013961","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":"Uncovering metabolic pathways in human alveolar macrophages in response to lipopolysaccharide.","authors":"Christine C A van Linge, Erik H A Michels, Liza Pereverzeva, Regina de Beer, Augustijn M Klarenbeek, Bauke V Schomakers, Michel van Weeghel, Riekelt H Houtkooper, W Joost Wiersinga, Peter I Bonta, Jouke T Annema, Tom van der Poll, Alex F de Vos","doi":"10.1093/cei/uxaf028","DOIUrl":"10.1093/cei/uxaf028","url":null,"abstract":"<p><strong>Introduction: </strong>Alveolar macrophages (AMs) play an essential role in maintaining homeostasis in the lung and in innate immunity for host defense. To fuel inflammatory responses, AMs do not rely on glycolysis, but require oxidative phosphorylation. However, which nutrients AMs use to fuel their energy demand during inflammatory responses, is still unknown. The present study aimed to determine the contribution of three key metabolic pathways; fatty acid oxidation, glutaminolysis, and glycogenolysis, to the inflammatory response of AMs.</p><p><strong>Methods: </strong>Primary AMs were isolated from healthy human volunteers and stimulated with lipopolysaccharide (LPS). After 24 hours, cells were subjected to analyses of metabolic flux, expression of genes involved in these metabolic pathways, and inflammatory cytokine secretion in the presence of metabolic inhibitors.</p><p><strong>Results: </strong>The results of our study show that human AMs display expression of genes involved in fatty acid and glutamine metabolism and are capable of metabolizing oleic acid and glutamine during homeostasis, but do not use these metabolites to fuel the production of inflammatory cytokines. We demonstrate that AMs, while residing in a glucose-deprived environment, contain glycogen and use glycogenolysis to fuel inflammatory cytokine secretion, as reflected by reduced TNF, IL-1β and IL-6 levels in supernatant of LPS-stimulated AMs treated with the glycogenolysis inhibitor CP316819. Moreover, AMs display marked expression of genes involved in glycogenesis, including FBP1 and GYS.</p><p><strong>Conclusions: </strong>Taken together, these results indicate that primary human AMs are equipped to use different nutrients to fuel their metabolic demands. Moreover, our findings suggest that glycogenolysis is critical for the inflammatory response of AMs.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12232543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293447","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":"Complement factors as biomarkers in ANCA-associated vasculitis in remission.","authors":"Rebecca Trattner, Maria Iordanou, Sophie Ohlsson, Myriam Martin, Mårten Segelmark, Anna M Blom","doi":"10.1093/cei/uxaf037","DOIUrl":"10.1093/cei/uxaf037","url":null,"abstract":"<p><strong>Background: </strong>Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a group of rare, autoimmune diseases causing inflammation in the vessel wall. Many organs can be affected, and kidney involvement is a common and serious manifestation. Complement activation is important in disease development and has also been detected in patients in remission. The reason for increased complement activation also without active disease is not understood.</p><p><strong>Methods: </strong>In this study, 65 AAV patients in remission, contributing with a total of 147 plasma samples, were included. Biomarkers of complement activation such as C4d (classical and lectin pathways), C3bBbP (alternative pathway), and soluble terminal complement complex (sTCC) (common terminal pathway) were measured with ELISA. For C4d measurement, an improved assay with an antibody targeting a cleavage neoepitope solely exposed during complement activation was used.</p><p><strong>Results: </strong>Our first hypothesis was that patients prone to recurrent flares might have an increased complement activation even when beeing in remission. However, we found no significant difference between those who did and did not develop flares during follow-up, nor any correlation between the total number of flares and any of the complement biomarkers. Interestingly, higher sTCC levels in remission correlated significantly to kidney involvement at the time of diagnosis and plasma creatinine levels at the time of sampling. Also, the diagnosis of microscopic polyangiitis (MPA), compared to granulomatosis with polyangiitis (GPA), yielded higher sTCC levels, and plasma C-reactive protein levels correlated significantly to sTCC.</p><p><strong>Conclusion: </strong>These findings suggest that persistent complement activation during remission in AAV may reflect underlying disease severity and organ involvement rather than predicting future flares.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12188287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144183662","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":"Role of a new truncated CD74 isoform in increased IL-17 secretion from stromal-immune cell interactions.","authors":"Mélissa Noack, Marlène Bailly, Laura Durix, Jean-Jacques Pin, Pierre Miossec","doi":"10.1093/cei/uxaf047","DOIUrl":"10.1093/cei/uxaf047","url":null,"abstract":"<p><strong>Introduction: </strong>Stromal-immune cell interactions promote pro-inflammatory cytokine secretion such as IL-17. IL-17 is involved in several chronic inflammatory diseases, affecting joints and skin. Podoplanin has been already identified as partially involved in high IL-17 secretion resulting from these cell interactions.</p><p><strong>Methods: </strong>The aim of this study was to identify new molecules, using co-cultures of activated peripheral blood mononuclear cells and synoviocytes (5:1 ratio). Cell interactions were critical to induce a high IL-17 production. The blockade of podoplanin inhibited this production, approximately 40%, confirming the contribution of other molecules. A battery of mouse monoclonal anti-human RA synoviocyte antibodies were tested in co-cultures and several were selected for their inhibitory effect on IL-17.</p><p><strong>Results: </strong>Cloning by expression allowed identifying the target of the selected 8350 antibody, a truncated isoform of CD74. CD74 blockade in co-cultures by 8350 antibody and a commercial antibody inhibited IL-17 production by 40%, but 8350 antibody had a limited effect on IL-10 inhibition. Furthermore, cell interactions increased CD74 expression, at mRNA and protein levels.</p><p><strong>Conclusion: </strong>This study identified truncated CD74 isoform as a novel molecule directly involved in high IL-17 secretion resulting from cell interactions. Inhibition of this truncated CD74 could represent a new therapeutic option for diseases with IL-17 involvement.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12342743/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144728354","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}