Scandinavian Journal of Immunology最新文献

Itaconate: A Potential Therapeutic Strategy for Autoimmune Disease. 衣康酸：一种治疗自身免疫性疾病的潜在策略。

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-05-01 DOI: 10.1111/sji.70026

Yifan Xie, Qi Cheng, Meng Li Xu, Jing Xue, Huaxiang Wu, Yan Du

{"title":"Itaconate: A Potential Therapeutic Strategy for Autoimmune Disease.","authors":"Yifan Xie, Qi Cheng, Meng Li Xu, Jing Xue, Huaxiang Wu, Yan Du","doi":"10.1111/sji.70026","DOIUrl":"https://doi.org/10.1111/sji.70026","url":null,"abstract":"Itaconate is a metabolite of the Krebs cycle, and endogenous itaconate is driven by a variety of innate signals that inhibit the production of inflammatory cytokines. The key mechanism of action of itaconate was initially found to be the competitive inhibition of succinate dehydrogenase (SDH), which inhibits the production of inflammatory factors, as well as its antioxidant effects. With increasing research, it was discovered that it modifies cysteine residues of related proteins through the Michael addition, such as modifying the Kelch-like ECH-associated protein 1 (KEAP1) protein and activating the nuclear factor erythroid 2-related factor 2 (NRF2) signalling pathway, as well as glycolytic enzymes and cellular pathway-associated factors that attenuate inflammatory responses and oxidative stress. It also acts on a variety of immune cells, affecting their function and activity, and has been increasingly shown to play a therapeutic role in a variety of inflammatory and autoimmune diseases through a combination of these mechanisms. In conclusion, there has been a great breakthrough in the research of itaconate, from the initial industrial application to the redefinition of the biological functions of itaconate. However, with the deepening of the research, we also found that there are more questions: the mechanism of action of itaconate, more functions of itaconate, clinical application of itaconate, and the use of itaconate still needs to be solved.","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"101 5","pages":"e70026"},"PeriodicalIF":4.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043949","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}

引用次数: 0

Upregulation of Fcγ Receptor IV on Activated Monocytes and Macrophages Causes Nonspecific Binding of the PK136 Anti-NK1.1 Antibody in Murine Models of Toll-Like Receptor-Induced Inflammation. 激活单核细胞和巨噬细胞上Fcγ受体IV的上调导致toll样受体诱导炎症小鼠模型中PK136抗nk1.1抗体的非特异性结合。

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-05-01 DOI: 10.1111/sji.70027

Amber De Visscher, Marte Vandeput, Bert Malengier-Devlies, Eline Bernaerts, Tania Mitera, Nele Berghmans, Philippe E Van den Steen, Carine Wouters, Patrick Matthys

{"title":"Upregulation of Fcγ Receptor IV on Activated Monocytes and Macrophages Causes Nonspecific Binding of the PK136 Anti-NK1.1 Antibody in Murine Models of Toll-Like Receptor-Induced Inflammation.","authors":"Amber De Visscher, Marte Vandeput, Bert Malengier-Devlies, Eline Bernaerts, Tania Mitera, Nele Berghmans, Philippe E Van den Steen, Carine Wouters, Patrick Matthys","doi":"10.1111/sji.70027","DOIUrl":"https://doi.org/10.1111/sji.70027","url":null,"abstract":"Nonspecific binding of monoclonal antibodies to Fcγ receptors (FcγRs) is a well-known root cause of unreliable results in flow cytometry. Over the past decade, liver Group 1 innate lymphoid cells (ILCs), including conventional natural killer (cNK) cells and type 1 ILCs (ILC1s), have been extensively studied by flow cytometry in various inflammatory liver disorders. In our previous work, we specifically evaluated changes in liver ILC1 numbers in two murine models of Toll-like receptor (TLR)-induced macrophage activation syndrome, a hyperinflammatory disorder with liver inflammation that is classified as a secondary form of hemophagocytic lymphohistiocytosis. Here, we follow up on a cell population that significantly expands during TLR triggering and resembles ILC1s, as they express CD49a and NK1.1 but lack expression of CD49b, a marker for cNK cells. However, detailed analysis revealed that these are CD49a+ monocytes/macrophages instead of ILC1s. During TLR triggering, their expression of FcγRIV increases significantly, leading to nonspecific binding of the frequently used PK136 anti-NK1.1 antibody, which cannot be blocked by standard Fcγ receptor blocking protocols. Instead, preincubation with anti-FcγRIV antibody or additional rat or mouse serum during antibody staining is necessary to prevent nonspecific anti-NK1.1 binding. Although we observed nonspecific binding of the anti-NK1.1 antibody in ex vivo applications, we confirmed that in vivo anti-NK1.1 only depletes truly NK1.1+ populations. In conclusion, we emphasise that studying NK1.1+ ILCs during inflammation by flow cytometry requires additional FcγRIV blocking reagents and careful exclusion of myeloid cells.","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"101 5","pages":"e70027"},"PeriodicalIF":4.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043950","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}

引用次数: 0

The Fusion Protein MuSK-Fc Functions as a Decoy to Block the Binding of Anti-MuSK Antibodies to MuSK. 融合蛋白麝香- fc可作为诱饵阻断抗麝香抗体与麝香的结合。

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-05-01 DOI: 10.1111/sji.70033

Akiyuki Uzawa, Hiroyuki Akamine, Manato Yasuda, Hideo Handa, Etsuko Ogaya, Kentaro Kurumada, Yosuke Onishi, Satoshi Kuwabara

引用次数: 0

Evaluation of the Impact of Anti-C1q Autoantibodies on Cardiovascular Outcomes in Systemic Lupus Erythematosus. 评价抗c1q自身抗体对系统性红斑狼疮心血管结局的影响。

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-05-01 DOI: 10.1111/sji.70028

Jessica S Kleer, Andrea Kieninger-Gräfitsch, Carlo Chizzolini, Uyen Huynh-Do, Camillo Ribi, Marten Trendelenburg

引用次数: 0

Fatigue in Inflammatory Bowel Disease: No Effect of Serum Concentrations of Infliximab, Adalimumab or Anti-Drug Antibodies During Maintenance Therapy. 炎症性肠病的疲劳：维持治疗期间英夫利昔单抗、阿达木单抗或抗药物抗体的血清浓度无影响

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-05-01 DOI: 10.1111/sji.70029

Tore Grimstad, Arne Carlsen, Jan Terje Kvaløy, Nils Bolstad, David John Warren, Lars Aabakken, Knut E A Lundin, Lars Karlsen, Øyvind Steinsbø, Roald Omdal

{"title":"Fatigue in Inflammatory Bowel Disease: No Effect of Serum Concentrations of Infliximab, Adalimumab or Anti-Drug Antibodies During Maintenance Therapy.","authors":"Tore Grimstad, Arne Carlsen, Jan Terje Kvaløy, Nils Bolstad, David John Warren, Lars Aabakken, Knut E A Lundin, Lars Karlsen, Øyvind Steinsbø, Roald Omdal","doi":"10.1111/sji.70029","DOIUrl":"https://doi.org/10.1111/sji.70029","url":null,"abstract":"Several studies have shown that infliximab and adalimumab ameliorate fatigue in inflammatory bowel disease. We investigated whether serum levels of these agents above or below a selected threshold influence fatigue severity. In this cross-sectional study, we measured serum concentrations (s-) of infliximab and adalimumab and corresponding anti-drug antibody levels. Therapeutic thresholds were defined as s-infliximab ≥ 5.0 mg/L and s-adalimumab ≥ 7.0 mg/L. Disease activity was assessed using the Harvey-Bradshaw Index for Crohn's disease, Partial Mayo Score for ulcerative colitis, and C-reactive protein (CRP) and faecal calprotectin levels for both conditions. Fatigue was assessed with the Fatigue Visual Analog Scale and Fatigue Severity Scale, and depression was evaluated with the Hospital Anxiety and Depression Scale, Depression subscale. Of 171 included patients (112 with Crohn's disease, 59 with ulcerative colitis), 66 (38.6%) were on infliximab and 105 (61.4%) were on adalimumab. Scores on the two fatigue scales were similar for serum values above versus below therapeutic thresholds for both drugs and did not differ with versus without anti-drug antibodies against either drug. CRP was numerically higher with infliximab levels below versus above the threshold (p = 0.06), whereas both CRP and faecal calprotectin were increased with adalimumab below versus above the threshold (p = 0.022, p = 0.0242). In patients with inflammatory bowel disease on maintenance therapy, s-infliximab and s-adalimumab levels below or above therapeutic thresholds or the presence of anti-drug antibodies did not affect fatigue severity. Trial Registration: ClinicalTrials.gov identifier: NCT02134054.","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"101 5","pages":"e70029"},"PeriodicalIF":4.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144019436","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}

引用次数: 0

Physiopathology of Allergic Asthma: A Comprehensive Review. 过敏性哮喘的生理病理：综述。

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-05-01 DOI: 10.1111/sji.70032

Najla Ghrairi, Youssef Zied Elhechmi

引用次数: 0

Inhibition of Alternative and Terminal Complement Pathway Components Modulate the Immune Response Against Bacteria and Fungi in Whole Blood. 抑制替代和终末补体途径成分调节全血中对细菌和真菌的免疫反应。

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-05-01 DOI: 10.1111/sji.70030

Leon Cyranka, Ida Mariegaard, Beatrice Fageräng, Laura Pérez-Alós, Verena Harpf, Tom Eirik Mollnes, Peter Garred, Anne Rosbjerg

{"title":"Inhibition of Alternative and Terminal Complement Pathway Components Modulate the Immune Response Against Bacteria and Fungi in Whole Blood.","authors":"Leon Cyranka, Ida Mariegaard, Beatrice Fageräng, Laura Pérez-Alós, Verena Harpf, Tom Eirik Mollnes, Peter Garred, Anne Rosbjerg","doi":"10.1111/sji.70030","DOIUrl":"10.1111/sji.70030","url":null,"abstract":"Complement activation plays a critical role in the inflammatory response to Escherichia coli and Aspergillus fumigatus conidia. However, the specific contributions of complement components, including anaphylatoxin receptors, remain unclear. Using an ex vivo lepirudin whole blood model, we examined the activation of all three complement pathways (C4c, C3bc, and sC5b-9) induced by these microbes. We also assessed granulocyte and monocyte receptor expression of CD11b, CD64, C3aR, C5aR1, and C5aR2, along with phagocytosis, leukocyte activation (MPO), and cytokine release. Additionally, we investigated selective inhibition of complement components FD, C3, C5, and C5aR1. Both microbes increased complement activation products (C3bc and sC5-9), CD11b and CD64 expression, MPO release, and proinflammatory cytokines (IL-1β, IL-6, IL-8, and TNF), while decreasing C3aR, C5aR1, and C5aR2 expression. Complement inhibition reduced CD11b and CD64 expression and partially restored C3aR and C5aR1 levels, with minimal effects on C5aR2. FD, C3, and C5 inhibition reduced downstream complement markers, with FD and C3 inhibition also reducing phagocytosis, and only C3 inhibition reducing MPO release. The cytokine response varied by microbe: E. coli triggered higher proinflammatory cytokines, and FD and C3 inhibition generally reduced cytokine release, while C5 inhibition was less effective. Interestingly, A. fumigatus-induced cytokines significantly increased with C5aR1 inhibition, highlighting immune response differences related to C5aR1 signalling in bacterial versus fungal infections. In conclusion, regulation of inflammation through FD, C3, C5, and C5aR1 underscores the immunoregulatory role of the complement system in anti-microbial immune responses.","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"101 5","pages":"e70030"},"PeriodicalIF":4.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12087264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094664","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}

引用次数: 0

Inflammatory Immune Markers Associated With Thyroid Peroxidase Autoantibodies in Children Diagnosed With Both Type 1 Diabetes and Celiac Disease. 与诊断为1型糖尿病和乳糜泻的儿童甲状腺过氧化物酶自身抗体相关的炎症免疫标志物

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-04-01 DOI: 10.1111/sji.70015

Emanuel Fryk, Andrea Tompa, Alexander Lind, Rasmus Bennet, Maria Faresjö

{"title":"Inflammatory Immune Markers Associated With Thyroid Peroxidase Autoantibodies in Children Diagnosed With Both Type 1 Diabetes and Celiac Disease.","authors":"Emanuel Fryk, Andrea Tompa, Alexander Lind, Rasmus Bennet, Maria Faresjö","doi":"10.1111/sji.70015","DOIUrl":"10.1111/sji.70015","url":null,"abstract":"Autoimmune thyroid disease (AITD) is associated with other autoimmune endocrine diseases such as type 1 diabetes (T1D) and celiac disease (CeD). Thyroid peroxidase autoantibodies (TPOA) are biomarkers of AITD but may also occur in patients with other autoimmune diseases. We examined cross-sectional correlations between TPOA and an array of immune markers in a cohort of 90 children with exclusively T1D (n = 27), CeD (n = 16) or a combination of these two diseases (n = 18), compared to a reference group of children without these diagnoses (n = 29). Children with exclusively T1D or T1D in combination with CeD had higher levels of TPOA with an overrepresentation among girls. The correlations between immune markers and TPOA were distinctly different between all study groups. In children with T1D, TPOA correlated mainly with the T helper 1 associated IFN-γ and pro-inflammatory IL-1β. In contrast, in children with combined diagnoses, TPOA was correlated with pro-inflammatory MCP-1, the acute phase proteins ferritin, fibrinogen, and serum albumin A, and adipocytokines resistin and visfatin. Children with exclusively CeD did not show the same strong association between immune markers and TPOA. In conclusion, TPOA positivity was mainly detected in patients with T1D and female sex. Several inflammatory markers correlated with TPOA, indicating a relation to autoimmune parameters in children with T1D, CeD or both, but preceding symptoms AITD.","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"101 4","pages":"e70015"},"PeriodicalIF":4.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11961787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764966","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}

引用次数: 0

Inflammasomes and Cardiovascular Disease: Linking Inflammation to Cardiovascular Pathophysiology. 炎症小体与心血管疾病：将炎症与心血管病理生理学联系起来。

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-04-01 DOI: 10.1111/sji.70020

Mohamed J Saadh, Faris Anad Muhammad, Rafid Jihad Albadr, Gaurav Sanghvi, S Renuka Jyothi, Mayank Kundlas, Kamal Kant Joshi, Akmal Rakhmatullaev, Waam Mohammed Taher, Mariem Alwan, Mahmood Jasem Jawad, Ali M Ali Al-Nuaimi

{"title":"Inflammasomes and Cardiovascular Disease: Linking Inflammation to Cardiovascular Pathophysiology.","authors":"Mohamed J Saadh, Faris Anad Muhammad, Rafid Jihad Albadr, Gaurav Sanghvi, S Renuka Jyothi, Mayank Kundlas, Kamal Kant Joshi, Akmal Rakhmatullaev, Waam Mohammed Taher, Mariem Alwan, Mahmood Jasem Jawad, Ali M Ali Al-Nuaimi","doi":"10.1111/sji.70020","DOIUrl":"10.1111/sji.70020","url":null,"abstract":"Cardiovascular diseases (CVDs) remain a leading cause of global mortality, driven by risk factors such as dyslipidemia, hypertension and diabetes. Recent research has highlighted the critical role of inflammasomes, particularly the NLRP3 inflammasome, in the pathogenesis of various CVDs, including hypertension, atherosclerosis, myocardial infarction and heart failure. Inflammasomes are intracellular protein complexes that activate inflammatory responses through the production of pro-inflammatory cytokines such as IL-1β and IL-18, contributing to endothelial dysfunction, plaque formation and myocardial injury. This review provides a comprehensive overview of the structure, activation mechanisms and pathways of inflammasomes, with a focus on their involvement in cardiovascular pathology. Key activation pathways include ion fluxes (K+ efflux and Ca2+ signalling), endoplasmic reticulum (ER) stress, mitochondrial dysfunction and lysosomal destabilisation. The review also explores the therapeutic potential of targeting inflammasomes to mitigate inflammation and improve outcomes in CVDs. Emerging strategies include small-molecule inhibitors, biologics and RNA-based therapeutics, with a particular emphasis on NLRP3 inhibition. Additionally, the integration of artificial intelligence (AI) in cardiovascular research offers promising avenues for identifying novel biomarkers, predicting disease risk and developing personalised treatment strategies. Future research directions should focus on understanding the interactions between inflammasomes and other immune components, as well as genetic regulators, to uncover new therapeutic targets. By elucidating the complex role of inflammasomes in CVDs, this review underscores the potential for innovative therapies to address inflammation-driven cardiovascular pathology, ultimately improving patient outcomes.","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"101 4","pages":"e70020"},"PeriodicalIF":4.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764963","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}

引用次数: 0

CD1d-iNKT Axis in Infectious Diseases: Lessons Learned From the Past. 传染病中的cd1 - inkt轴：从过去的经验教训。

IF 4.1 4区医学

Scandinavian Journal of Immunology Pub Date : 2025-04-01 DOI: 10.1111/sji.70024

Priyajit Chatterjee, Shubhranil Brahma, Peter Cresswell, Syamdas Bandyopadhyay

{"title":"CD1d-iNKT Axis in Infectious Diseases: Lessons Learned From the Past.","authors":"Priyajit Chatterjee, Shubhranil Brahma, Peter Cresswell, Syamdas Bandyopadhyay","doi":"10.1111/sji.70024","DOIUrl":"https://doi.org/10.1111/sji.70024","url":null,"abstract":"CD1d is an antigen-presenting molecule that presents lipid or glycolipid antigens to iNKT cells, a distinct subset of T lymphocytes characterised by their innate-like properties and restricted use of Vα, Jα and Vβ segments. The CD1d-iNKT axis represents an interesting aspect of the immune system with significant potential for therapeutic interventions against infectious diseases. Upon recognition of lipid antigens, iNKT cells initiate rapid and potent immune responses, releasing a diverse array of cytokines such as IL-4, IL-13, IFN-γ etc. that profoundly influence immune reactions against various pathogens, including bacteria and parasites, bridging innate and adaptive immunity. We identify and describe the key features of lipidic antigens and their derivatives that determine the nature of their antigenicity. Furthermore, modulating CD1d-driven iNKT cell responses by an array of lipid and glycolipid antigens holds promise as adjunctive therapy to existing antimicrobial treatments. Understanding the complexities of the CD1d-iNKT axis and exploiting its therapeutic potential in the case of infectious diseases could lead to innovative immunotherapeutic strategies, ushering in a new era of immunotherapy against pathogenic insults.","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"101 4","pages":"e70024"},"PeriodicalIF":4.1,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144046504","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}

引用次数: 0