Journal of Innate Immunity最新文献_第5页

Unraveling the Intricate Web: Complement Activation Shapes the Pathogenesis of Sepsis-Induced Coagulopathy. 揭开错综复杂的网络：补体激活决定败血症诱发凝血病的发病机制

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-05-31 DOI: 10.1159/000539502

Xin Wei, Ye Tu, Shuhong Bu, Guimei Guo, Hongbin Wang, Zhibin Wang

{"title":"Unraveling the Intricate Web: Complement Activation Shapes the Pathogenesis of Sepsis-Induced Coagulopathy.","authors":"Xin Wei, Ye Tu, Shuhong Bu, Guimei Guo, Hongbin Wang, Zhibin Wang","doi":"10.1159/000539502","DOIUrl":"10.1159/000539502","url":null,"abstract":"Background: Sepsis-associated coagulopathy specifically refers to widespread systemic coagulation activation accompanied by a high risk of hemorrhage and organ damage, which in severe cases manifests as disseminated intravascular coagulation (DIC), or even develops into multiple organ dysfunction syndrome (MODS). The complement system and the coagulation system as the main columns of innate immunity and hemostasis, respectively, undergo substantial activation after sepsis.Summary: Dysfunction of the complement, coagulation/fibrinolytic cascades caused by sepsis leads to \"thromboinflammation,\" which ultimately amplifies the systemic inflammatory response and accelerates the development of MODS. Recent studies have revealed that massive activation of the complement system exacerbates sepsis-induced coagulation and even results in DIC, which suggests that inhibition of complement activation may have therapeutic potential in the treatment of septic coagulopathy.Key messages: Sepsis-associated thrombosis involves the upregulation or activation of procoagulant factors, down-regulation or inactivation of anticoagulant factors, and impairment of the fibrinolytic mechanism. This review aims to summarize the latest literature and analyze the underlying molecular mechanisms of the activation of the complement system on the abnormal coagulation cascades in sepsis.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"337-353"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11249610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141179136","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}

引用次数: 0

TLR2 and NLRP3 Orchestrate Regulatory Roles in Escherichia coli Infection-Induced Septicemia in Mouse Models. TLR2 和 NLRP3 在大肠埃希菌感染诱发的小鼠模型败血症中发挥调节作用。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-10-15 DOI: 10.1159/000541819

Zhiguo Gong, Wei Mao, Jiamin Zhao, Peipei Ren, Zhuoya Yu, Yunjie Bai, Chao Wang, Yuze Liu, Shuang Feng, Surong Hasi

{"title":"TLR2 and NLRP3 Orchestrate Regulatory Roles in Escherichia coli Infection-Induced Septicemia in Mouse Models.","authors":"Zhiguo Gong, Wei Mao, Jiamin Zhao, Peipei Ren, Zhuoya Yu, Yunjie Bai, Chao Wang, Yuze Liu, Shuang Feng, Surong Hasi","doi":"10.1159/000541819","DOIUrl":"10.1159/000541819","url":null,"abstract":"Introduction: Escherichia coli (E. coli) is a significant commensal gram-negative bacterium that can give rise to various diseases. The roles of Toll-like receptor 2 (TLR2) and the NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome in sepsis induced by E. coli infection remain unclear.Methods: In vivo, we investigated differences in mortality, production of inflammatory mediators, organ damage, neutrophil count, and bacterial load during E. coli infection in C57BL/6J mice, as well as in mice deficient in TLR2 or NLRP3. In vitro, we investigated the impact of E. coli on the activation of TLR2 and NLRP3 in macrophages and the influence of TLR2 and NLRP3 on the activation of inflammatory signaling pathways and the secretion of inflammatory mediators in macrophages induced by E. coli infection.Results: TLR2-deficient (TLR2-/-) and NLRP3-deficient (NLRP3-/-) mice exhibit significantly increased mortality and organ damage after E. coli infection. These mice also show elevated levels of TNF-α and IL-10 in serum and peritoneal lavage fluid. Additionally, TLR2-/- and NLRP3-/- mice display heightened neutrophil recruitment and increased bacterial load in the blood. Furthermore, macrophages from these mice demonstrate a significant reduction in the activation of the MAPK signaling pathway.Conclusion: TLR2 and NLRP3 play crucial roles in modulating inflammatory mediator expression, immune cell recruitment, and bactericidal activity, thereby preventing excessive tissue damage and reducing mortality in E. coli-induced sepsis.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"513-528"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11548895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142467606","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}

引用次数: 0

Immunometabolic Regulation of Bacterial Infection, Biofilms, and Antibiotic Susceptibility. 细菌感染、生物膜和抗生素敏感性的免疫代谢调节。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-02-03 DOI: 10.1159/000536649

Ying-Tsun Chen, Gaurav Kumar Lohia, Samantha Chen, Sebastián A Riquelme

{"title":"Immunometabolic Regulation of Bacterial Infection, Biofilms, and Antibiotic Susceptibility.","authors":"Ying-Tsun Chen, Gaurav Kumar Lohia, Samantha Chen, Sebastián A Riquelme","doi":"10.1159/000536649","DOIUrl":"10.1159/000536649","url":null,"abstract":"Background: Upon infection, mucosal tissues activate a brisk inflammatory response to clear the pathogen, i.e., resistance to disease. Resistance to disease is orchestrated by tissue-resident macrophages, which undergo profound metabolic reprogramming after sensing the pathogen. These metabolically activated macrophages release many inflammatory factors, which promote their bactericidal function. However, in immunocompetent individuals, pathogens like Pseudomonas aeruginosa, Staphylococcus aureus, and Salmonella evade this type of immunity, generating communities that thrive for the long term.Summary: These organisms develop features that render them less susceptible to eradication, such as biofilms and increased tolerance to antibiotics. Furthermore, after antibiotic therapy withdrawal, \"persister\" cells rapidly upsurge, triggering inflammatory relapses that worsen host health. How these pathogens persisted in inflamed tissues replete with activated macrophages remains poorly understood.Key messages: In this review, we discuss recent findings indicating that the ability of P. aeruginosa, S. aureus, and Salmonella to evolve biofilms and antibiotic tolerance is promoted by the similar metabolic routes that regulate macrophage metabolic reprogramming.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"143-158"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10914382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139681200","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}

引用次数: 0

Obituary of Prof. Uli Theopold, 1957-2023. 乌利-西奥波德教授的讣告，1957-2023。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-01-08 DOI: 10.1159/000535642

Ylva Engström, Bruno Lemaitre, Dan Hultmark

引用次数: 0

Role of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 in Inflammation and Pathogen-Associated Interactions. 胶原蛋白样氧化低密度脂蛋白受体-1（LOX-1）在炎症和病原体相关相互作用中的作用。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-01-17 DOI: 10.1159/000535793

Sarah Truthe, Tilman E Klassert, Stefan Schmelz, Danny Jonigk, Wulf Blankenfeldt, Hortense Slevogt

{"title":"Role of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 in Inflammation and Pathogen-Associated Interactions.","authors":"Sarah Truthe, Tilman E Klassert, Stefan Schmelz, Danny Jonigk, Wulf Blankenfeldt, Hortense Slevogt","doi":"10.1159/000535793","DOIUrl":"10.1159/000535793","url":null,"abstract":"Background: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is known as a major receptor for oxidized low-density lipoproteins (oxLDL) and plays a significant role in the genesis of atherosclerosis. Recent research has shown its involvement in cancer, ischemic stroke, and diabetes. LOX-1 is a C-type lectin receptor and is involved in the activation of immune cells and inflammatory processes. It may further interact with pathogens, suggesting a role in infections or the host's response.Summary: This review compiles the current knowledge of potential implications of LOX-1 in inflammatory processes and in host-pathogen interactions with a particular emphasis on its regulatory role in immune responses. Also discussed are genomic and structural variations found in LOX-1 homologs across different species as well as potential involvements of LOX-1 in inflammatory processes from the angle of different cell types and organ-specific interactions.Key messages: The results presented reveal both similar and different structures in human and murine LOX-1 and provide clues as to the possible origins of different modes of interaction. These descriptions raise concerns about the suitability, particularly of mouse models, that are often used in the analysis of its functionality in humans. Further research should also aim to better understand the mostly unknown binding and interaction mechanisms between LOX-1 and different pathogens. This pursuit will not only enhance our understanding of LOX-1 involvement in inflammatory processes but also identify potential targets for immunomodulatory approaches.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"105-132"},"PeriodicalIF":5.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10866614/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139485735","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}

引用次数: 0

Eosinophils Are an Endogenous Source of Interleukin-4 during Filarial Infections and Contribute to the Development of an Optimal T Helper 2 Response. 嗜酸性粒细胞是丝虫感染期间 IL-4 的内源性来源，有助于形成最佳的 T 辅助细胞 2 反应。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-02-26 DOI: 10.1159/000536357

Cécile Guth, Pia Philippa Schumacher, Archena Vijayakumar, Hannah Borgmann, Helene Balles, Marianne Koschel, Frederic Risch, Benjamin Lenz, Achim Hoerauf, Marc P Hübner, Jesuthas Ajendra

{"title":"Eosinophils Are an Endogenous Source of Interleukin-4 during Filarial Infections and Contribute to the Development of an Optimal T Helper 2 Response.","authors":"Cécile Guth, Pia Philippa Schumacher, Archena Vijayakumar, Hannah Borgmann, Helene Balles, Marianne Koschel, Frederic Risch, Benjamin Lenz, Achim Hoerauf, Marc P Hübner, Jesuthas Ajendra","doi":"10.1159/000536357","DOIUrl":"10.1159/000536357","url":null,"abstract":"Introduction: Interleukin-4 (IL-4) is a central regulator of type 2 immunity, crucial for the defense against multicellular parasites like helminths. This study focuses on its roles and cellular sources during Litomosoides sigmodontis infection, a model for human filarial infections.Methods: Utilizing an IL-4 secretion assay, investigation into the sources of IL-4 during the progression of L. sigmodontis infection was conducted. The impact of eosinophils on the Th2 response was investigated through experiments involving dblGATA mice, which lack eosinophils and, consequently, eosinophil-derived IL-4.Results: The absence of eosinophils notably influenced Th2 polarization, leading to impaired production of type 2 cytokines. Interestingly, despite this eosinophil deficiency, macrophage polarization, proliferation, and antibody production remained unaffected.Conclusion: Our research uncovers eosinophils as a major source of IL-4, especially during the early phase of filarial infection. Consequently, these findings shed new light on IL-4 dynamics and eosinophil effector functions in filarial infections.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"159-172"},"PeriodicalIF":5.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10932553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139735439","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}

引用次数: 0

TLRs1-10 Protein Expression in Circulating Human White Blood Cells during Bacterial and COVID-19 Infections. 细菌和 COVID-19 感染期间循环人白细胞中的 TLRs1-10 蛋白表达。

IF 4.7 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2024-03-08 DOI: 10.1159/000536593

Louise Chomel, Mathieu Vogt, Julien Demiselle, Pierrick Le Borgne, Marine Tschirhart, Valentin Morandeau, Hamid Merdji, Laurent Miguet, Julie Helms, Ferhat Meziani, Laurent Mauvieux

{"title":"TLRs1-10 Protein Expression in Circulating Human White Blood Cells during Bacterial and COVID-19 Infections.","authors":"Louise Chomel, Mathieu Vogt, Julien Demiselle, Pierrick Le Borgne, Marine Tschirhart, Valentin Morandeau, Hamid Merdji, Laurent Miguet, Julie Helms, Ferhat Meziani, Laurent Mauvieux","doi":"10.1159/000536593","DOIUrl":"10.1159/000536593","url":null,"abstract":"Introduction: Toll-like receptors play crucial roles in the sepsis-induced systemic inflammatory response. Septic shock mortality correlates with overexpression of neutrophilic TLR2 and TLR9, while the role of TLR4 overexpression remains a debate. In addition, TLRs are involved in the pathogenesis of viral infections such as COVID-19, where the single-stranded RNA of SARS-CoV-2 is recognized by TLR7 and TLR8, and the spike protein activates TLR4.Methods: In this study, we conducted a comprehensive analysis of TLRs 1-10 expressions in white blood cells from 71 patients with bacterial and viral infections. Patients were divided into 4 groups based on disease type and severity (sepsis, septic shock, moderate, and severe COVID-19) and compared to 7 healthy volunteers.Results: We observed a significant reduction in the expression of TLR4 and its co-receptor CD14 in septic shock neutrophils compared to the control group (p < 0.001). Severe COVID-19 patients exhibited a significant increase in TLR3 and TLR7 levels in neutrophils compared to controls (p < 0.05). Septic shock patients also showed a similar increase in TLR7 in neutrophils along with elevated intermediate monocytes (CD14+CD16+) compared to the control group (p < 0.005 and p < 0.001, respectively). However, TLR expression remained unchanged in lymphocytes.Conclusion: This study provides further insights into the mechanisms of TLR activation in various infectious conditions. Additional analysis is needed to assess their correlation with patient outcome and to evaluate the impact of TLR-pathway modulation during septic shock and severe COVID-19.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"216-225"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140094203","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}

引用次数: 0

Association of Vitamin D with Severity and Outcome of COVID-19: Clinical and Experimental Evidence. 维生素D与COVID-19严重程度和结局的关系:临床和实验证据

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2024-01-01 Epub Date: 2023-11-26 DOI: 10.1159/000535302

Georgios Renieris, Spyros Foutadakis, Theano Andriopoulou, Victoria-Marina Spanou, Dionyssia-Eirini Droggiti, Dionysios Kafousopoulos, Theologia Gkavogianni, Georgia Damoraki, Giannis Vatsellas, Evangelos J Giamarellos-Bourboulis

{"title":"Association of Vitamin D with Severity and Outcome of COVID-19: Clinical and Experimental Evidence.","authors":"Georgios Renieris, Spyros Foutadakis, Theano Andriopoulou, Victoria-Marina Spanou, Dionyssia-Eirini Droggiti, Dionysios Kafousopoulos, Theologia Gkavogianni, Georgia Damoraki, Giannis Vatsellas, Evangelos J Giamarellos-Bourboulis","doi":"10.1159/000535302","DOIUrl":"10.1159/000535302","url":null,"abstract":"Introduction: The role of vitamin in COVID-19 remains controversial. We investigated the association between endogenous vitamin D and the severity of COVID-19 as well as the mechanisms of action of vitamin D supplementation.Methods: 25(OH)D3 in serum was associated with disease severity and outcome in 190 COVID-19 patients. In a COVID-19 animal model using intravenous injection of plasma from patients with COVID-19 acute respiratory distress syndrome into C57/BL6 mice, mice were treated with 0.25 μg human 1,25(OH)D3 or vehicle. Mice were sacrificed on day 4. Cytokines and myeloperoxidase (MPO) in tissues were measured. Changes in gene expression after vitamin D supplementation were measured.Results: Vitamin D deficiency and insufficiency were associated with increased severity and unfavorable outcome after 28 days. Vitamin D levels were negatively associated with biomarkers of COVID-19 severity. Vitamin D supplementation after challenge of mice with COVID-19 plasma led to reduced levels of TNFα, IL-6, IFNγ, and MPO in the lung, as well as down-regulation of pro-inflammatory pathways.Conclusion: Normal levels of endogenous vitamin D are associated with reduced severity and risk of unfavorable outcome in COVID-19, possibly through attenuation of tissue-specific hyperinflammation.","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"1-11"},"PeriodicalIF":5.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10764091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138440779","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}

引用次数: 0

C-X-C motif chemokine ligand 1 promotes colitis by modulating the gut microbiota C-X-C motif趋化因子配体 1 通过调节肠道微生物群促进结肠炎的发生

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-12-08 DOI: 10.1159/000535637

Hang Zhao, Wenhua Li, Xin Zhou, Liang Pan, Yun Feng, Pingyu Gao, Jie Ji, Huanyan Zhang, Kai Zhao, Chi Wang, Zhanjun Lu

{"title":"C-X-C motif chemokine ligand 1 promotes colitis by modulating the gut microbiota","authors":"Hang Zhao, Wenhua Li, Xin Zhou, Liang Pan, Yun Feng, Pingyu Gao, Jie Ji, Huanyan Zhang, Kai Zhao, Chi Wang, Zhanjun Lu","doi":"10.1159/000535637","DOIUrl":"https://doi.org/10.1159/000535637","url":null,"abstract":"Introduction: C-X-C motif chemokine ligand 1 (CXCL1) is a potent neutrophil chemoattractant that plays a pivotal role in recruiting neutrophils during inflammatory conditions. This study explored the role of CXCL1 in modulating the gut microbiota, influencing neutrophil infiltration, and contributing to the development of colitis. \u0000Methods: We employed quantitative PCR to assess CXCL1 expression in colon samples. A mouse model of DSS-induced colitis was utilized to explore the progression of colitis in wild-type (WT) and CXCL1-deficient (CXCL1-/-) mice. \u0000Results: Colitis attenuation was evident in CXCL1-/- mice. Significant alterations were observed in the gut microbiome, as revealed by 16S rRNA gene sequencing. Furthermore, CXCL1-/- mice exhibited reduced gut permeability and diminished endotoxin levels in peripheral blood following DSS treatment compared to WT mice. In response to DSS treatment, WT mice showed a clear increase in neutrophil infiltration, while CXCL1-/- mice exhibited lower levels of infiltration. FMT using stools from CXCL1-/- mice alleviated DSS-induced colitis. Interestingly, FMT from patients with colitis increased CXCL1 and Ly6G expression in colons of gut-sterilized mice. Clinical data analysis revealed elevated CXCL1 and CD15 expression in patients with colitis, with a positive correlation between the severity of colitis and the expression of CXCL1 and CD15. \u0000Conclusion: These findings shed light on the pivotal role of CXCL1 in promoting colitis by modulating the gut microbiota.\u0000","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":"53 30","pages":""},"PeriodicalIF":5.3,"publicationDate":"2023-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138587955","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}

引用次数: 0

Erratum. 勘误表。

IF 5.3 3区医学

Journal of Innate Immunity Pub Date : 2023-05-15 DOI: 10.1159/000530893

引用次数: 0