Bruno Griesler, Marijke Hölzel, Jana Oswald, Johannes Fänder, Trutz Fischer, Maximilian Büttner, Dagmar Quandt, Ina Bähr, Simon Jasinski-Bergner, Ivonne Bazwinsky-Wutschke, Heike Kielstein
{"title":"Impact of siRNA-Mediated Cofilin-1 Knockdown and Obesity Associated Microenvironment on the Motility of Natural Killer Cells.","authors":"Bruno Griesler, Marijke Hölzel, Jana Oswald, Johannes Fänder, Trutz Fischer, Maximilian Büttner, Dagmar Quandt, Ina Bähr, Simon Jasinski-Bergner, Ivonne Bazwinsky-Wutschke, Heike Kielstein","doi":"10.1080/08820139.2024.2327327","DOIUrl":"10.1080/08820139.2024.2327327","url":null,"abstract":"<p><p>The anti-tumor capacity of natural killer (NK) cells heavily relies on their ability to migrate towards their target cells. This process is based on dynamic actinrearrangement, so-called actin treadmilling, andis tightly regulated by proteins such as cofilin-1. The aim of the present study was to identify the role of cofilin-1 (CFL-1) in the migratory behavior of NK cells and to investigate a possible impact of an obesity-associated micromilieu on these cells, as it is known that obesity correlates with various impaired NK cell functions. CFL-1 was knocked-down via transfection of NK-92 cells with respective siRNAs. Obesity associated micromilieu was mimicked by incubation of NK-92 cells with adipocyte-conditioned medium from human preadipocyte SGBS cells or leptin. Effects on CFL-1 levels, the degree of phosphorylation to the inactive pCFL-1 as well as NK-92 cell motility were analyzed. Surprisingly, siRNA-mediated CFL-1 knockdown led to a significant increase of migration, as determined by enhanced velocity and accumulated distance of migration. No effect on CFL-1 nor pCFL-1 expression levels, proportion of phosphorylation and cell migratory behavior could be demonstrated under the influence of an obesity-associated microenvironment. In conclusion, the results indicate a significant effect of a CFL-1 knockdown on NK cell motility.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"713-729"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140896076","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}
Yasser B M Ali, Mai M Saed, Nehal E Abdel-Hakem, Mona Abd Elmotaleb A Hussein, Mohamed El-Shahat
{"title":"Genetic Association of Interleukin 16 Gene Polymorphisms (rs11556218 & rs4778889) with Type 1 Diabetes in Egyptian Children: A Case-Control Study.","authors":"Yasser B M Ali, Mai M Saed, Nehal E Abdel-Hakem, Mona Abd Elmotaleb A Hussein, Mohamed El-Shahat","doi":"10.1080/08820139.2024.2349034","DOIUrl":"10.1080/08820139.2024.2349034","url":null,"abstract":"<p><strong>Background: </strong>Type 1 diabetes (T1D) is a serious chronic autoimmune condition. Even though the underlying reason for the onset of T1D is unknown, due to their effector and regulatory roles in immune responses, cytokines are essential in developing autoimmune disorders. Interleukin (IL)16 is an immunomodulatory cytokine implicated in several inflammatory and autoimmune diseases.</p><p><strong>Objective: </strong>This study was designed to examine the association of IL16 gene polymorphisms, rs11556218 T > G and rs4778889 T > C, with the risk of T1D in Egyptian children.</p><p><strong>Methods: </strong>Using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay, we analyzed rs11556218 T > G and rs4778889 T > C polymorphisms of the IL16 gene in 100 T1D subjects and 93 controls.</p><p><strong>Results: </strong>Rs11556218 T > G polymorphism of the IL16 gene was not associated with the risk of developing T1D. Analysis of IL16 gene rs4778889 T > C showed that the TT genotype had a considerably higher risk of T1D than the TC genotype [OR = 2.195 (1.205-3.999)]. In comparison to patients with the C allele [OR = 0.6914 (0.38-1.2569)], patients with the T allele [OR = 1.45 (0.7956-2.6296)] were notably more likely to have T1D. A significant decrease was found in the frequency of GT (OR = 0.43, <i>p</i> = .03) and TC (OR = 0.32, <i>p</i> = .011) haplotypes of IL16 gene rs11556218 T > G and rs4778889 T > C polymorphisms in T1D patients compared with controls.</p><p><strong>Conclusion: </strong>IL16 gene rs4778889 T > C polymorphism might be associated with susceptibility to T1D. Egyptians with TT genotypes are more likely to develop T1D. However, GT and TC haplotypes of IL16 gene rs11556218 T > G and rs4778889 T > C polymorphisms highlight their protective role againstT1D disease.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"830-842"},"PeriodicalIF":2.9,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075926","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}
{"title":"Betulinic Acid Potentiates Mast Cell Degranulation by Compromising Cell Membrane Integrity and Without Involving Fcεri Receptors.","authors":"Gouse M Shaik, Mohd Shahnawaz Khan","doi":"10.1080/08820139.2024.2329990","DOIUrl":"10.1080/08820139.2024.2329990","url":null,"abstract":"<p><p>Mast cells play important role in acquired and natural immunity making these favorable therapeutic targets in various inflammatory diseases. Here we observed that, pentacyclic tri terpenoid betulinic acid (BA) treatment resulted in a significantly high number (9%) of cells positive for Hoechst and negative for annexin-V indicating that BA could interfere with plasma membrane integrity. The degranulation of both activated and non-activated mast cells was enhanced upon treatment with BA. The pre-treatment of BA had remarkable effect on calcium response in activated mast cells which showed increased calcium influx relative compared to untreated cells. The results also showed potentially less migration of BA treated mast cells signifying the possible effect of BA on cell membrane. BA treatment resulted in a significant increase in mRNA levels of IL-13 while as mRNA levels of other target cytokines, IL-6 and TNF-α seem to be not affected. Moreover, there was global Increase in phosphorylation of signaling proteins and no significant change in phosphorylation of FcεRI receptors indicating that the effect of BA was independent of signaling cascade or FcεRI receptor mediated mast cell aggregation. Overall, these results portray BA potentiates mast cell effector functions by compromising the membrane integrity and independent of FcεRI involvement.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"695-711"},"PeriodicalIF":2.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140174521","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}
Juan Lu, Qingguo Ren, Weiwei Qi, Ning Yang, Yuanyuan He
{"title":"The Clinical Significance and the Potential Regulatory Mechanism of the LncRNA OIP5-AS1 in Paediatric Severe Community-Acquired Pneumonia Blood Through the MiR-150-5p/PDCD4 Axis.","authors":"Juan Lu, Qingguo Ren, Weiwei Qi, Ning Yang, Yuanyuan He","doi":"10.1080/08820139.2024.2309557","DOIUrl":"10.1080/08820139.2024.2309557","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to elucidate the clinical significance and regulatory mechanism of the long non-coding RNA OIP5-AS1 in severe community-acquired pneumonia (SCAP) among paediatric patients.</p><p><strong>Methods: </strong>qRT-PCR was used to assess the mRNA levels of OIP5-AS1. ROC curve analysis was used to assess the diagnostic significance of OIP5-AS1. Short-term prognostic significance was evaluated through Kaplan-Meier survival. An in vitro cell model was developed using LPS-induced MRC-5 cells. CCK-8, flow cytometry, and ELISA were conducted to measure cell viability, apoptosis, and inflammatory factor levels. The association between miR-150-5p and PDCD4 was confirmed through DLR assays.</p><p><strong>Results: </strong>Elevated OIP5-AS1 were observed in paediatric patients with SCAP, which enabled effective differentiation from healthy individuals. High expression of OIP5-AS1 correlated with reduced survival rates. OIP5-AS1 knockdown attenuated cell viability suppression and the promotion of apoptosis and inflammatory factors induced by LPS. However, this attenuation was reversed by reduced levels of miR-150-5p. miR-150-5p was identified as a target of PDCD4 and OIP5-AS1.</p><p><strong>Conclusion: </strong>Increased OIP5-AS1 levels show potential as a valuable diagnostic and prognostic biomarker for paediatric patients with SCAP. This study illustrates its role in regulating cell viability, apoptosis, and the inflammatory response via the miR-150-5p/PDCD4 axis, acting as a ceRNA.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"541-558"},"PeriodicalIF":2.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139641972","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}
Xiaoyi Dong, Zhimao Ye, Cuiping Li, Kongmei Li, Xiaoxia Zhong, Hao Li
{"title":"Mogroside Ⅴ Inhibits M1 Polarization and Inflammation of Diabetic Mouse Macrophages via p38 MAPK/NF-Κb Signaling Pathway.","authors":"Xiaoyi Dong, Zhimao Ye, Cuiping Li, Kongmei Li, Xiaoxia Zhong, Hao Li","doi":"10.1080/08820139.2024.2321353","DOIUrl":"10.1080/08820139.2024.2321353","url":null,"abstract":"<p><strong>Background: </strong>Mogroside V (MV) has anti-inflammatory properties. However, its impact on macrophage polarization under diabetic condition is yet unclear. This study aimed to investigate effects and underlying mechanisms of MV on inflammatory response and M1 polarization of bone marrow-derived macrophages (BMDMs) from diabetic mice.</p><p><strong>Methods: </strong>BMDMs were isolated from normal and diabetic C57BL/6 mice. LPS and IFN-γwere used to produce M1-polarized BMDMs. MV treatment was administered throughout the M1 polarization process with or without SB203580 or PDTC. Surface markers CD11b, F4/80 and CD86 of macrophages were identified using flow cytometry or immunofluorescence staining. Inflammatory cytokines IL-1β and IL-6 and phosphorylation levels of p65 and p38 were examined by western blot.</p><p><strong>Results: </strong>High glucose increased proportion of CD11b<sup>+</sup>F4/80<sup>+</sup>CD86<sup>+</sup> cells, protein levels of inflammatory cytokines IL-1β and IL-6 and phosphorylation levels of p65 and p38 in LPS+IFN-γ-induced BMDMs, while they were decreased upon MV treatment. Additionally, these effects were further downregulated when MV was co-added with SB203580 or PDTC.</p><p><strong>Conclusions: </strong>MV suppressed M1 macrophage polarization and inflammatory response, which was partially through NF-κB and p38 MAPK in LPS+IFN-γ induced BMDMs under high glucose condition, implying the potential of MV in treatment for inflammatory complications of diabetes.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"604-621"},"PeriodicalIF":2.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139982881","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}
Jie Pang, Yanxia Li, Ran Tao, Jing Li, Feifei Wang, Huaheng Xu
{"title":"Correlation Between B-Cell Activating Factor of the Tumor Necrosis Factor Family Level in Serum and Immune Inflammation in Patients with Neuropsychiatric Systemic Lupus Erythematosus and its Clinical Value.","authors":"Jie Pang, Yanxia Li, Ran Tao, Jing Li, Feifei Wang, Huaheng Xu","doi":"10.1080/08820139.2024.2309567","DOIUrl":"10.1080/08820139.2024.2309567","url":null,"abstract":"<p><strong>Objective: </strong>Neuropsychiatric systemic lupus erythematosus (NPSLE) is a form of SLE associated with severe NP syndromes causing mortality and morbidity. Respecting the fundamental of BAFF in NPSLE pathophysiology, we investigated its clinical value.</p><p><strong>Methods: </strong>Totally 105 NPSLE and 101 SLE cases without NPSLE (non-NPSLE, control) were included. Serum BAFF/TNF-α/IL-6/IL-10 levels were measured using ELISA kits. T lymphocytes were detected by flow cytometry. The independent influencing factors for NPSLE, and the auxiliary diagnostic efficacy and the ability of BAFF levels to predict adverse prognosis of NPSLE patients were analyzed by multiple factor logistic regression, and ROC curve and survival curve.</p><p><strong>Results: </strong>In NPSLE patients, serum BAFF level was increased and positively correlated with SLEDAI-2k, serum proinflammatory cytokines, while negatively correlated with CD4+T/CD8+T cells, and anti-inflammatory cytokine. High serum BAFF protein level was associated with a higher risk of developing NPSLE. The AUC of serum BAFF > 301.7 assisting in NPSLE diagnosis was 0.8196. Furthermore, high levels of serum BAFF were associated with a higher risk of adverse outcomes in NPSLE patients. .</p><p><strong>Conclusion: </strong>Serum BAFF level in NPSLE patients was correlated with lymphocytes and high serum BAFF protein level could assist in diagnosis and to predict adverse outcomes in NPSLE patients.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"559-573"},"PeriodicalIF":2.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139702434","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}
{"title":"Retraction: Polymorphisms in CD14 Gene May Modify Soluble CD14 Levels and Represent Risk Factors for Multiple Sclerosis.","authors":"","doi":"10.1080/08820139.2024.2346369","DOIUrl":"10.1080/08820139.2024.2346369","url":null,"abstract":"","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"712"},"PeriodicalIF":2.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141065253","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}
Liou Huang, Chunrong Wu, Dan Xu, Yuhui Cui, Jianguo Tang
{"title":"IL1RAP Exacerbates Sepsis-Induced Pulmonary and Spleen Injury Through Regulating CD4<sup>+</sup> T Lymphocyte Differentiation.","authors":"Liou Huang, Chunrong Wu, Dan Xu, Yuhui Cui, Jianguo Tang","doi":"10.1080/08820139.2024.2312898","DOIUrl":"10.1080/08820139.2024.2312898","url":null,"abstract":"<p><strong>Background: </strong>Complex pathophysiological the specific mechanism of sepsis on CD4<sup>+</sup> T-cell responses is less well understood. IL1 receptor accessory protein (IL1RAP) was found to be involved in activating host immune responses.</p><p><strong>Method: </strong>Cecum ligation and puncture (CLP) was utilized to build a mouse sepsis model. The experiment was randomly divided into four groups: Sham, CLP, CLP + shNC, and CLP + shIL1RAP group.</p><p><strong>Results: </strong>qRT-PCR suggested mRNA levels of IL1RAP were decreased when IL1RAP was knocked down with the mRNA levels of IL-1β, NF-κB, and p38 decreased. Histopathology showed severe pathological damage with alveolar integrity lost, red blood cells in the alveoli, massive inflammatory cell infiltration, and the alveolar wall was thickening in the CLP group. The inflammatory cytokine levels of TNF-α, IL-1β, and IFN-γ were elevated in CLP mice by ELISA. The counts of CD4<sup>+</sup> T cells were decreased in sepsis mice in peripheral blood, spleen, and BALF by flow cytometry. However, the above was blocked down when using shIL1RAP. Western blot suggested sh IL1RAP inhibited IL-1β, NF-κB, and p38 protein expressions.</p><p><strong>Conclusions: </strong>We defined IL1RAP as a new target gene through NF-κB/MAPK pathways regulating CD4<sup>+</sup> T lymphocyte differentiation mediated the progression of sepsis, which is potentially exploitable for immunotherapy.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"574-585"},"PeriodicalIF":2.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139702435","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}
Mehrdad Farrokhi, Pedram Moeini, Mohammad Fazilati, Habibollah Nazem, Shahla Faraji, Zahra Saadatpour, Elyas Fadaei, Leila Saadatpour, Ali Rezaei, Sadra Ansaripour, Ali Amani-Beni
{"title":"RETRACTED ARTICLE: Polymorphisms in CD14 Gene May Modify Soluble CD14 Levels and Represent Risk Factors for Multiple Sclerosis.","authors":"Mehrdad Farrokhi, Pedram Moeini, Mohammad Fazilati, Habibollah Nazem, Shahla Faraji, Zahra Saadatpour, Elyas Fadaei, Leila Saadatpour, Ali Rezaei, Sadra Ansaripour, Ali Amani-Beni","doi":"10.1080/08820139.2016.1226897","DOIUrl":"10.1080/08820139.2016.1226897","url":null,"abstract":"<p><p>Statement of RetractionWe, the Editors and Publisher of the journal <i>Immunological Investigations</i>, have retracted the following article:Merhdad Farrokhi, Pedram Moeini, Mohammada Fazilati, Habibollah Nazem, Shahla Faraji, Zahra Saadatpour, Elyas Fadaei, Leila Saadatpour, Ali Rezaei, Sadra Ansaripour and Ali Amani-Beni (2016) Polymorphisms in CD14 Gene May Modify Soluble CD14 Levels and Represent Risk Factors for Multiple Sclerosis, <i>Immunological Investigations</i>, DOI: https://doi.org/10.1080/08820139.2016.1226897Since publication, significant concerns have been raised about the author affiliations, ethical approval, and the integrity of the data in the article.When approached for an explanation, the authors provided responses to our queries regarding the flow cytometry data, but they have not sufficiently addressed all of our concerns. In particular, the authors and institution did not respond to our requests for proof that the research was conducted at the Isfahan University of Medical Sciences or provide proof of ethical approval.As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. The corresponding author listed in this publication has been informed.We have been informed in our decision-making by our Editorial Policies and COPE guidelines.The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as 'Retracted'.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":"1 1","pages":"I-VIII"},"PeriodicalIF":2.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59792696","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}
Alma Celeste Ortega-Rodriguez, Paola Del Carmen Guerra de Blas, Ricardo Ramírez-Torres, Elena B Martínez-Shio, Adriana E Monsiváis-Urenda
{"title":"Quantitative Analysis of Innate Lymphoid Cells in Patients with ST-Segment Elevation Myocardial Infarction.","authors":"Alma Celeste Ortega-Rodriguez, Paola Del Carmen Guerra de Blas, Ricardo Ramírez-Torres, Elena B Martínez-Shio, Adriana E Monsiváis-Urenda","doi":"10.1080/08820139.2024.2316052","DOIUrl":"10.1080/08820139.2024.2316052","url":null,"abstract":"<p><strong>Background: </strong>Acute myocardial infarction (AMI) is one of the principal causes of death in Mexico and worldwide. AMI triggers an acute inflammatory process that induces the activation of different populations of the innate immune system. Innate lymphoid cells (ILCs) are an innate immunity, highly pleiotropic population, which have been observed to participate in tissue repair and polarization of the adaptive immune response.</p><p><strong>Objective: </strong>We aimed to analyze the levels of subsets of ILCs in patients with ST-segment elevation myocardial infarction (STEMI), immediately 3 and 6 months post-AMI, and analyze their correlation with clinical parameters.</p><p><strong>Results: </strong>We evaluated 29 STEMI patients and 15 healthy controls and analyzed the different subsets of circulating ILCs, immediately 3 and 6 months post-AMI. We observed higher levels of circulating ILCs in STEMI patients compared to control subjects and a significant correlation between ILC levels and cardiac function. We also found increased production of the cytokines interleukin 5 (IL-5) and interleukin 17A (IL-17A), produced by ILC2 cells and by ILC3 cells, respectively, in the STEMI patients.</p><p><strong>Conclusion: </strong>This study shows new evidence of the role of ILCs in the pathophysiology of AMI and their possible involvement in the maintenance of cardiac function.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"586-603"},"PeriodicalIF":2.8,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140867669","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}