Clinical and experimental immunology最新文献

{"title":"The small molecule inhibitor 3PO is a modulator of neutrophil metabolism, ROS production, and NET release.","authors":"Michele Fresneda Alarcon, Genna Ali Abdullah, Andy Nolan, Christina Linford, Maria Martina Meschis, Andrew L Cross, Andrew Sellin, Marie M Phelan, Helen L Wright","doi":"10.1093/cei/uxaf012","DOIUrl":"10.1093/cei/uxaf012","url":null,"abstract":"<p><p>Neutrophils are key effector leukocytes of the innate immune system and play a pivotal role in defending the host against microbial infections. Recent studies have identified a crucial link between glycolysis and neutrophil cellular functions. Using human neutrophils, we have investigated the intricate relationship between glycolysis, extracellular glucose availability, and the enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), in the regulation of reactive oxygen species (ROS) and neutrophil extracellular trap (NET) production. We have identified that PFKFB3 is elevated in rheumatoid arthritis (RA) neutrophils and that the small molecule PFKFB3 inhibitor 3PO is a key regulator of neutrophil ROS and NET production. 3PO blocked the production of ROS and NETs in a dose-dependent manner in both RA and healthy neutrophils (P < 0.01), and RA neutrophils were more sensitive to lower concentrations of 3PO. Bacterial killing was only partially inhibited by 3PO, and the proportion of live neutrophils after 24 h incubation was unchanged. Using NMR metabolomics, we identified that 3PO increases the concentration of lactate, phenylalanine, and L-glutamine in neutrophils, as well as significantly decreasing intracellular glutathione (adj. P-value < 0.05). We also demonstrated that RA neutrophils produce ROS and NETs in culture conditions which mimic the low glucose environments encountered in RA synovial joints. Our results also suggest that 3PO may have molecular targets beyond PFKFB3. By dissecting the intricate interplay between metabolism and neutrophil effector functions, this study advances the understanding of the molecular mechanisms governing pro-inflammatory neutrophil responses and identifies 3PO as a potential therapeutic for conditions characterized by dysregulated neutrophil activation.</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/PMC12060009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143447662","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":"Immune-modulatory effects of Spindlin-1 inhibitors.","authors":"Susanne Schiffmann, Marina Henke, Friedemann Weber, Michael J Parnham","doi":"10.1093/cei/uxaf013","DOIUrl":"10.1093/cei/uxaf013","url":null,"abstract":"<p><p>Spindlin-1, a multivalent epigenetic reader, is a new target for cancer therapy. Beside the anticancer effect, modulation of the recognition of methyl marks of histones may impact the immune system, which plays an important role in the anticancer strategy of the human organism. Two Spindlin-1 inhibitors (A366, MS31) were characterized to differentiate between drug and target-specific effects. We performed a comprehensive study regarding the influence of Spindlin-1 inhibition on various immune cells. A366 and MS31 showed immune cell type-dependent cytotoxicity with IC50 values in the ranges of 37-143 µM and 11-3122 µM, respectively, macrophages tending to be less susceptible than lymphocytes. A366 had only minor effects on M1 polarization, whereas MS31 shifted the M1 to a M2 phenotype, as shown by regulated cytokines and surface marker expression. Both A366 and MS31 weakened the polarization of predifferentiated M2 macrophages by reducing surface marker expression, cytokines, and inflammatory markers. A366 and MS31 had no effect on activation and energy metabolism of CD4+ T cells. Interestingly, 5 µM A366 and 2.5 µM MS31 clearly prevented B cell activation, as shown by reduced proliferation, plasmablast formation, and release of immunoglobulins A and G. Additionally, A366 increased energy metabolism in B cells. In conclusion, the inhibition of Spindlin-1 had only minor effects on polarization of macrophages and T cell proliferation but profoundly prevented B cell activation at low concentrations. This suggests that Spindlin-1 inhibitors, while mediating anticancerogenic effects, may also suppress the humoral immune response and increase infection risk.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":"219 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12164290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282715","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 potential of autologous patient-derived circulating extracellular vesicles to improve drug delivery in rheumatoid arthritis.","authors":"Ori Moskovitch, Adi Anaki, Tal Caller, Boris Gilburd, Ori Segal, Omer Gendelman, Abdulla Watad, Ruty Mehrian-Shai, Yael Mintz, Shlomo Segev, Yehuda Shoenfeld, Rachela Popovtzer, Howard Amital, Gilad Halpert","doi":"10.1093/cei/uxae101","DOIUrl":"10.1093/cei/uxae101","url":null,"abstract":"<p><p>Recognizing the need for innovative therapeutic approaches in the management of autoimmune diseases, our current investigation explores the potential of autologous extracellular vesicles (EVs), derived from the blood of rheumatoid arthritis patients, to serve as therapeutic vectors to improve drug delivery. We found that circulating EVs derived from arthritic mice (collagen-induced arthritis model) express the joint/synovia homing receptor, αVβ3 integrin. Importantly, both autologous labeled EVs, derived from the blood of arthritic mice (collagen antibody-induced arthritis model) and healthy mice-derived EVs, exhibit targeted migration toward inflamed synovia without infiltrating healthy joints, as demonstrated by an in vivo imaging system. Furthermore, EVs derived from plasma of rheumatoid arthritis patients show an overexpression of αV integrin and are effectively taken up by lipopolysaccharides/tumor necrosis factor alpha (TNFα)-induced activated human synovial cell line in vitro, although interestingly the uptake of healthy EVs was found to be significantly increased. Notably, arthritic mice-derived circulating EVs, strongly express murine glucose transporter 1, which in turn can facilitate their binding to glucose-coated gold nanoparticles (previously shown to be conjugated with drugs for improved drug delivery). The significance of our results, lies in the identification of autologous tissue homing EVs as promising vectors, offering a novel avenue to enhance targeted delivery of anti-inflammatory/rheumatic drugs in rheumatoid arthritis treatment.</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/PMC11754864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930717","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":"Peripheral immune biomarkers associated with response to adoptive cell therapy with tumor infiltrating lymphocytes.","authors":"Cecilie Oelvang Madsen, Marta Velasco Santiago, Evelina Martinenaite, Troels Holz Borch, Marco Donia, Inge Marie Svane, Morten Hansen","doi":"10.1093/cei/uxaf010","DOIUrl":"10.1093/cei/uxaf010","url":null,"abstract":"<p><p>Adoptive cell therapy (ACT) with ex-vivo expanded tumor-infiltrating lymphocytes (TILs, TIL-ACT) has shown clinical efficacy in a significant proportion of patients with metastatic melanoma. To further target TIL-ACT toward responsive patients, identifying predictive biomarkers and understanding broader immune dynamics remain critical. This study investigated the peripheral blood immune landscape in 47 patients with metastatic melanoma undergoing TIL-ACT, assessing antitumor reactivity and peripheral immune cell profiles before and after treatment. Responders displayed increased frequency of circulating tumor-reactive cells post-treatment, and higher baseline levels of activated CD57-expressing T cells, serving as potential biomarkers of response. In contrast, persistent high serum levels of interleukin (IL)-6 and IL-8, higher frequencies of CD38-expressing T cells, and regulatory T cells (Tregs) post-treatment, correlated with unfavorable outcomes. These findings contribute to understanding the peripheral immune landscape associated with response to TIL-ACT, offering valuable insights into predictive biomarkers and mechanisms to improve patient selection.</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/PMC12010344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143447646","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":"Comprehensive flow cytometry-based diagnosis of XIAP deficiency.","authors":"Dan Tomomasa, Madoka Nishimura, Ayami Ohya, Kay Tanita, Ryosuke Wakatsuki, Ryohei Watanabe, Satoshi Miyamoto, Akihiro Hoshino, Takahiro Kamiya, Takeshi Isoda, Shuya Kaneko, Masaki Shimizu, Atsushi Hijikata, Katsuhide Eguchi, Masataka Ishimura, Yukako Maeda, Kazushi Izawa, Takaaki Meguro, Kosuke Fujimoto, Etsuko Ishikita-Murayama, Kyogo Suzuki, Eri Okura, Tomoko Uehara, Tomotada Takayama, Satoshi Okada, Masatoshi Takagi, Tomohiro Morio, Rebecca A Marsh, Hirokazu Kanegane","doi":"10.1093/cei/uxaf020","DOIUrl":"10.1093/cei/uxaf020","url":null,"abstract":"<p><p>Deficiency of X-linked inhibitor of apoptosis protein (XIAP) is an X-linked recessive inborn error of immunity characterized by abnormal immune responses leading to inflammatory bowel disease and hemophagocytic lymphohistiocytosis. Although XIAP protein expression analysis by flow cytometry (XIAP flow) is commonly used to diagnose XIAP deficiency, certain variants may not affect the protein expression, thereby complicating the diagnostic process. XIAP is crucial for the nucleotide-binding and oligomerization domain 2 (NOD2) signaling pathway. In this study, we aimed to perform a comprehensive analysis of nine patients diagnosed with XIAP deficiency through genetic testing. In addition to XIAP flow, we employed a previously reported method utilizing muramyl dipeptide (MDP) stimulation, a specific agonist of NOD2, to quantitatively evaluate the downstream tumor necrosis factor-alpha (TNFα) production by flow cytometry in patient monocytes (MDP flow). The median mean fluorescence intensity in healthy controls with XIAP flow was 711 (95% confidence interval [CI], 653-815) compared to 195 (95% CI, 161-386) in patients with XIAP deficiency (P < 0.0001). The median percentage of TNFα-producing monocytes in controls with MDP flow was 29.1% (95% CI, 19.6-53.7), while in patients it was 0.34% (95% CI, 0.18-0.82) (P = 0.0008). The receiver operating characteristic curves demonstrated that both XIAP flow and MDP flow exhibited 100% sensitivity and specificity. Taken together, combining XIAP flow and MDP flow analyses allows for a highly accurate diagnosis.</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/PMC12062573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699630","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":"Sulforaphane relieved inflammation symptoms in EAP mice by blocking oxidative stress and NLRP3 inflammasome activation through the Nrf2 pathway.","authors":"Tong Meng, Rui Feng, Yunlong Zhu, Jincheng Luo, Andong Zhang, Yi Liu, Jing Chen, Cheng Yang","doi":"10.1093/cei/uxaf022","DOIUrl":"10.1093/cei/uxaf022","url":null,"abstract":"<p><p>Chronic prostatitis and chronic pelvic pain syndrome (CP/CPPS) are diagnosed in patients with various pelvic or genitourinary symptoms irrespective of the presence of a tender prostate. The etiology of chronic nonbacterial prostatitis remains unclear. Current treatments such as alpha-blockers, neuroleptics, anti-inflammatory, medications, and physical therapy, are often unsatisfactory. New treatments, as well as an improved knowledge of the underlying CP/CPPS pathogenesis, are thus needed. Sulforaphane (SFN), an isothiocyanate found in large quantities in Brassica species, has shown therapeutic effects on inflammation and cancer, and can protect against DNA damage and modulate the cell cycle to control apoptosis, angiogenesis, and metastasis. At the molecular level, SFN modulates cell homeostasis by activating the transcription factor Nrf2. However, its effect on CP/CPPS is not clear. Here, SFN was found to alleviate inflammation by suppressing NLRP3 inflammasomes via the Nrf2/HO-1 axis, as demonstrated in both animal and cellular analyses.</p>","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":"219 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12070798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966072","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":"Characterization of T-bet expressing B cells in lupus patients indicates a putative prognostic and therapeutic value of these cells for the disease.","authors":"Athanasios Sachinidis, Maria Trachana, Anna Taparkou, George Gavriilidis, Vasileios Vasileiou, Sofoklis Keisaris, Panayotis Verginis, Christina Adamichou, Dimitrios Boumpas, Fotis Psomopoulos, Alexandros Garyfallos","doi":"10.1093/cei/uxaf008","DOIUrl":"10.1093/cei/uxaf008","url":null,"abstract":"<p><strong>Objective: </strong>To investigate whether T-bet+ B cells, as well as age-associated B cells/ABCs (CD19 + CD21-CD11c + T-bet+) and double-negative B cells/DN (CD19 + IgD-CD27- CXCR5-T-bet+), serve as prognostic and/or therapeutic tools for systemic lupus erythematosus (SLE) in humans.</p><p><strong>Methods: </strong>Flow cytometry was used for enumerating T-bet+ B cells and ABCs/DN subsets, found in the peripheral blood of 10 healthy donors and 22 active SLE patients. Whole blood assay cultures, combined with in vitro pharmacological treatments, were performed to evaluate the effects of hydroxychloroquine, anifrolumab, and fasudil (a ROCK kinase inhibitor) on T-bet+ B cells' percentage. Moreover, previously published single-cell RNA sequencing (scRNA-seq) data were used in a meta-analysis to allow characterization of genes and pathways associated with the biology of T-bet in B cells.</p><p><strong>Results: </strong>T-bet+ B cells displayed an expansion in SLE patients [1.47 (1.9-0.7) vs 10.85 (37.4-3.6)]. Similarly, both ABCs and DN were found to be expanded. Interestingly, percentages of T-bet+ B cells positively correlated with patients' SLEDAI scores (rs = 0.55, P = 0.007). Cell culture experiments conducted revealed that all three agents tested can deplete T-bet + B cells (without affecting the cell viability of lymphocytes, T cells, and B cells). According to bioinformatics analyses, T-bet is highly expressed in two B-cell clusters with pathogenic characteristics for SLE (designated as atypical memory B cells and activated naïve B cells). These clusters can be targeted for therapeutic interventions.</p><p><strong>Conclusions: </strong>T-bet+ B cells can serve as a putative prognostic biomarker of lupus severity. Circumstantial data suggest that these cells may promote disease pathogenesis and may represent a novel therapeutic target.</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/PMC12062963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370588","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":"Mouse CD8+ T cell subsets differentially generate IL-17-expressing cells in the colon epithelium and lamina propria.","authors":"Cunjin Ge, Qiaoyun Tong, Shihua Zheng, Lei Liu, Lugao Tian, Hesheng Luo","doi":"10.1093/cei/uxae120","DOIUrl":"10.1093/cei/uxae120","url":null,"abstract":"<p><p>Colon-resident CD8+ T cells actively contribute to gut homeostasis and the pathogenesis of inflammatory bowel disease. However, their heterogeneity in generating IL-17-expressing CD8+ T cells, i.e. Tc17 cells, has not been thoroughly revealed. This study aims to characterize the abilities of mouse colonic intraepithelial (IE) and lamina propria (LP) CD8+ T cell subsets to differentiate into Tc17 cells. Using flow cytometry, we found that normal TCRβ+CD4-CD8αα+ cells (CD8αα T cells) and TCRβ+CD4-CD8αβ T cells, (CD8αβ T cells), either IE or LP, expressed abundant granzymes and IFN-γ but minute IL-17A. Under the in vitro Tc17-inducing condition, IE CD8αα T cells showed the weakest Tc17 differentiation ability and LP CD8αβ T cells exhibited the strongest Tc17 differentiation ability, whereas IE CD8αβ T cells and LP CD8αα T cells demonstrated moderate Tc17 differentiation abilities. The expression of IL-6 receptor, TGF-β receptor, TCR signaling indicators, CD161, and IL-23 receptor was low in IE CD8αα T cells, median in IE CD8αβ T cells and LP CD8αα T cells, but high in LP CD8αβ T cells. IE CD8αα T cells weakly induced the expression of chemokines, cytokines, and host defense mediators in colonic epithelial cells while LP CD8αβ T cells showed a robust up-regulatory effect. Furthermore, these colonic CD8+ T cell subsets also exhibited different abilities to generate Tc17 cells in inflamed colons. Collectively, LP CD8αβ T cells have the strongest Tc17 differentiation ability and might play a more significant role than the other subsets in Tc17-mediated immunity or inflammation in the colon.</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/PMC11780888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920821","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":"FcγRIIB (CD32B) antibodies enhance immune responses through activating FcγRs.","authors":"Alexander P Simpson, Robert J Oldham, Kerry L Cox, Martin C Taylor, Sonya James, Ann L White, Yury Bogdanov, Martin J Glennie, Björn Frendeus, Mark S Cragg, Ali Roghanian","doi":"10.1093/cei/uxaf015","DOIUrl":"10.1093/cei/uxaf015","url":null,"abstract":"<p><p>Fc receptors (FcR) play a key role in coordinating responses from both the innate and adaptive immune system. The inhibitory Fc gamma receptor (FcγRIIB/CD32B; referred to as FcγRII/CD32 in mice) restrains the immune response, specifically through regulating immunoglobulin G (IgG) effector functions. FcγRII-deficient mice demonstrate elevated incidence and severity of autoimmunity and increased responses to immunization and infections. To explore the potential of FcγRIIB as a target for augmenting vaccines, we tested the ability of monoclonal antibodies (mAb) against mouse FcγRII and human FcγRIIB to enhance humoral responses in preclinical models. We used wild-type (WT), FcγR-deficient, and human FcγRIIB transgenic (Tg) mice with either a functional intracellular domain (hFcγRIIB Tg) or lacking immunoreceptor tyrosine-based inhibitory motif (ITIM) signalling capacity (NoTIM). Targeting mouse FcγRII and human FcγRIIB with antibodies significantly augmented humoral immune responses against experimental antigens and enhanced tumour clearance in vivo. Surprisingly, mAbs without a functional Fc (N297Q; referred to as Fc-null) lacked efficacy. Similarly, blocking FcγRII in mice lacking activating FcγRs failed to enhance immune responses. Conversely, blocking both signalling-competent and signalling-defective (NoTIM) FcγRIIB in Tg mice with a WT, but not Fc-null, FcγRIIB mAb equally enhanced immunity. These data indicate the redundancy of inhibitory signalling in potentiating immune responses in vivo. Collectively, our data suggest that mAb-targeting of FcγRIIB stabilizes mAb Fc and enhances immune responses via Fc-mediated crosslinking of activating FcγRs, irrespective of the inhibitory function of FcγRIIB. These findings support a strategy to boost immune responses in immunization protocols.</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/PMC12046127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633517","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: Essential role of interferon-regulatory factor 4 in regulating diabetogenic CD4+ T and innate immune cells in autoimmune diabetes in NOD mice.","authors":"","doi":"10.1093/cei/uxaf032","DOIUrl":"10.1093/cei/uxaf032","url":null,"abstract":"","PeriodicalId":10268,"journal":{"name":"Clinical and experimental immunology","volume":"219 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233369","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}