Innate Immunity最新文献

{"title":"Retraction: The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal goblet cell dysfunction.","authors":"","doi":"10.1177/17534259261427520","DOIUrl":"10.1177/17534259261427520","url":null,"abstract":"","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261427520"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12932873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283589","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}

{"title":"Immune cells play a mediating role in the relationship between the gut microbiota and dementia: A Mendelian randomization study.","authors":"Jianzhun Chen, Liuhui Zhu, Jie Liu, Jieyu Chen, Chunyu Liang, Chenxi Liu, Fang Wang, Yongyun Zhu, Xinglong Yang","doi":"10.1177/17534259261426829","DOIUrl":"10.1177/17534259261426829","url":null,"abstract":"<p><p>IntroductionThe gut microbiota modulates dementia pathogenesis through immune interactions. Using Mendelian randomization, we investigate immune mediated mechanisms linking microbial dysbiosis to four dementia subtypes (Alzheimer's disease, Frontotemporal dementia, Vascular dementia, Parkinson's disease dementia . Our study tests whether gut microbiome effects on dementia are transmitted via immunoregulatory pathways.MethodsGenome wide association studies data included gut microbiota, 731 immune traits, and dementia cohorts (Alzheimer's disease, Frontotemporal dementia, Vascular dementia, Parkinson's disease dementia). Two step Mendelian randomization with Inverse Variance Weighted analyses assessed mediation effects, controlled by F-statistics >10 and Steiger filtering. Sensitivity analyses addressed pleiotropy<b>.</b>ResultsA total of 37 gut microbiome species demonstrated potential causal effects relationships with four types of dementia, and 137 immune cell subsets exhibited potential causal effects associations with these four dementia subtypes. In the Two step Mendelian randomization analysis, CD45RA + CD28- CD8+ T cells, CD19 on IgD- CD38dim B cells, and BAFF-R on CD20- B cells were shown to exert mediating effects between <i>class/order/family.Deltaproteobacteria</i> and Alzheimer's disease. CD4+ CD8+ T cells were found to exert a mediating effect between <i>genus.Roseburia</i> and Parkinson's disease dementia . CD20- CD38- B cells, CD19 on CD20- B cells, and IgD on unswitched memory B cells were found to exert a mediating effect between <i>class/order/family.Coriobacteriales,genus.Lactococcus</i> and Vascular dementia.ConclusionThis Mendelian randomization study revealed that certain immune cells serve as mediators in the pathway by which the gut microbiome contributes to the onset of dementia.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261426829"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12932898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283529","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}

{"title":"Advancing lupus nephritis research through multi-omics and predictive modeling.","authors":"Lisha Mou, Ying Lu, Zijing Wu, Zuhui Pu","doi":"10.1177/17534259261426818","DOIUrl":"10.1177/17534259261426818","url":null,"abstract":"<p><p>IntroductionLupus nephritis (LN) is characterized by significant heterogeneity and a complex pathophysiology, which traditional methods struggle to fully resolve. Advanced multi-omics approaches are essential to disentangle its cellular and molecular drivers.MethodsWe employed an integrative strategy combining single-cell RNA sequencing (scRNA-seq) profiling of LN biopsies with large-scale bulk RNA-seq cohorts. We applied non-negative matrix factorization (NMF) to scRNA-seq data to define robust immune meta-programs and utilized CellChat to decode cell-cell communication networks. Leveraging these insights to overcome sample size limitations, we prioritized key pathways and developed 399 machine learning predictive models using bulk transcriptomics, validated on independent cohorts.ResultsScRNA-seq analysis revealed a distinct cellular landscape, including a rare population of plasmacytoid dendritic cells (pDCs) and an expanded population of CD56dimCD16⁺ natural killer (NK) cells expressing high levels of IFN-γ and perforin, suggesting a role in inflammatory pathology. Macrophage subpopulation CM2 emerged as a central pro-inflammatory hub, potentially driving fibrosis via autocrine signaling and epithelial activation. We observed reduced Treg-B cell interactions, suggesting a regulatory collapse. Our machine learning models, based on innate immunity, circadian rhythms, apoptosis, and NF-κB signaling, achieved high diagnostic accuracy (AUC = 0.929 for innate immunity). Hub genes, including <i>CYBB</i>, <i>CSF2RB</i>, and <i>IRF8</i>, were confirmed to be upregulated in LN and correlated with clinical severity in external validation datasets. Molecular docking simulations suggested a potential structural basis for CYBB-dexamethasone interaction, providing a hypothesis for future verification.DiscussionThis study identifies CM2 macrophages and dysregulated pDC-NK axes as key drivers of LN. By bridging cellular interactomes with clinical predictive modeling, we provide a robust roadmap for precision detection and identifying potential therapeutic targets in LN.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261426818"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13133451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770603","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}

{"title":"Periodontitis promotes gingival accumulation of cells with MDSC phenotype.","authors":"Fernando García-Arévalo, Gabriela Leija-Montoya, Dulce Martha Fuchen-Ramos, Javier González-Ramírez, Mario Isiordia-Espinoza, Nicolas Serafin-Higuera","doi":"10.1177/17534259261422539","DOIUrl":"10.1177/17534259261422539","url":null,"abstract":"<p><p>BackgroundPeriodontitis is one of the most common inflammatory diseases in humans, mostly caused by bacterial infection and with diverse populations of immune cells involved. Myeloid-derived suppressor cells (MDSCs), a heterogeneous group of immature myeloid cells derived from hematopoietic precursor cells, have exhibited immunomodulatory functions by production of different molecules such as inducible NO synthase (iNOS) and it is thought to be involved in periodontitis. However, reports of characterization of cells with MDSC phenotypes in gingival tissues are very scarce. This study aimed to characterize gingival cells with MDSC phenotypes in healthy gingiva and periodontitis tissues.Methods and ResultsHuman healthy gingival tissues and those with periodontitis were included to analyze cells with MDSC phenotypes by flow cytometry. Additionally, a mouse model of experimental periodontitis was used to identify cells with MDSC phenotypes and production of iNOS. Results showed an increased accumulation of CD45⁺HLA-DR^neg/lowCD11b⁺CD33⁺ cells in human gingival tissues with periodontitis. Experimental periodontitis promotes accumulation of CD45⁺CD11b⁺Gr-1⁺ and CD45⁺CD11b⁺Ly6G⁺ cells in gingival tissues. Experimental periodontitis did not promote accumulation of these subpopulations in other tissues as spleen. Additionally, gingival CD45⁺Gr-1⁺ iNOS⁺ cells were identified.Conclusionscells with MDSC phenotypes are resident in healthy gingival tissues and their accumulation is locally triggered by periodontitis. Cells with capacity of iNOS production could be implicated in generation of reactive nitrogen species, suggesting immunomodulatory properties.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261422539"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12909751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146201546","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}

{"title":"Endothelial progenitor cell numbers vary in newborns and adults; anti-gm-CSFα (CD116) antibody as a novel marker for EPC enumeration.","authors":"Sevil Simsek, Cagatay Karaca, Nezihe Koker, Adnan Öztürk, Mustafa Yavuz Koker","doi":"10.1177/17534259261438615","DOIUrl":"10.1177/17534259261438615","url":null,"abstract":"<p><p>ObjectiveEndothelial progenitor cells (EPCs) originate from hematopoietic stem cells and can be quantified in peripheral blood using flow cytometry. The anti-GM-CSFα antibody (CD116) may serve as a specific marker for EPC enumeration. This study aimed to quantify peripheral EPCs expressing CD116 and compare the results with other specific antibodies in newborns and adults.Materials and MethodsEPC enumeration was performed by flow cytometric analysis of peripheral blood leukocytes (PBLs) obtained from 50 individuals, including 25 newborns and 25 adults. A CD34-specific antibody was used to identify hematopoietic stem/progenitor cells, while an antibody panel consisting of CD116, CD146, CD31, and CD45 was employed for EPC identification.ResultsEnumeration of CD34⁺ hematopoietic progenitor cells (HPCs) demonstrated that the mean CD34⁺ HPC count per 10⁶ PBLs was 1643 (935-1458) in newborns and 242.7 (163-190) in adults, with a statistically significant difference between the groups (<i>p</i> < 0.001). Using CD146 staining, the mean number of circulating EPCs per 10⁶ PBLs was 94.2 (90.5-129.0) in newborns and 9.2 (7.4-12.4) in adults (<i>p</i> < 0.001). Similarly, enumeration based on CD31 staining revealed mean EPC counts of 19.0 (12.5-28.0) in newborns and 6.0 (5.0-7.0) in adults (<i>p</i> < 0.001). Enumeration using CD116 staining showed mean EPC numbers of 29.0 (23.0-34.0) in newborns and 3.0 (2.0-4.0) in adults, also indicating a significant difference between the two groups (<i>p</i> < 0.001).ConclusionEPC numbers are significantly higher in newborns than in adults, suggesting an important developmental role for these cells. The GM-CSFα-specific antibody (CD116) may serve as a novel auxiliary marker for the identification and quantification of circulating EPCsubpopulations. Furthermore, EPC numbers appear to vary across different life stages, with higher numbers in newborns potentially reflecting the presence of a highly regenerative microenvironment.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261438615"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13070191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645267","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}

{"title":"Retraction: Effect of berberine on LPS-induced expression of NF-κB/MAPK signalling pathway and related inflammatory cytokines in porcine intestinal epithelial cells.","authors":"","doi":"10.1177/17534259261435238","DOIUrl":"10.1177/17534259261435238","url":null,"abstract":"","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261435238"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13018703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147511569","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}

{"title":"The role of trained immunity in chronic non-communicable inflammatory diseases.","authors":"Joseph Mucumbitsi, Jean Claude Hakizimana, Marie Gorette Kampire, Callixta Kaneza, Themistocles Bushobozi, Sophie Mukantwari, Jean Mfizi Ngaboyishema, Alex Butera, Abdullateef Isiaka Alagbonsi","doi":"10.1177/17534259261446050","DOIUrl":"https://doi.org/10.1177/17534259261446050","url":null,"abstract":"<p><p>BackgroundTrained immunity, a form of long-term functional reprogramming of innate immune cells through epigenetic and metabolic changes, traditionally confers protection against infections. However, inappropriate activation by endogenous sterile stimuli can drive persistent maladaptive inflammation in non-communicable diseases (NCDs).ObjectiveThis systematic review synthesizes primary evidence for trained immunity in atherosclerosis, type 2 diabetes mellitus (T2DM), chronic kidney disease (CKD), and neurodegenerative disorders, focusing on endogenous inducers, cellular mediators, mechanisms, and translational implications.Data Sources and MethodsFollowing PRISMA guidelines, we included original studies demonstrating trained immunity induced by sterile endogenous signals in the targeted diseases. Narrative synthesis was performed due to heterogeneity precluding meta-analysis.ResultsTwelve primary studies met the inclusion criteria. In atherosclerosis (n = 8 studies), oxLDL, aldosterone, Western diet lipids, and post-myocardial infarction signals induced trained immunity in monocytes or macrophages and hematopoietic progenitors via H3K4me3 enrichment, mTOR/NLRP3 activation, and glycolytic/fatty acid shifts, leading to persistent cytokine hyperproduction (TNF-α, IL-6), foam cell formation, and transmissible plaque progression. In T2DM/hyperglycemia (n = 3), high glucose levels triggered MLL-mediated epigenetic reprogramming and glycolysis-dependent \"metabolic memory,\" which skewed myelopoiesis and accelerated atherosclerosis despite normoglycemia. In CKD (n = 1), indoxyl sulfate induced AhR-dependent arachidonic acid pathway activation with metabolic rewiring, sustaining systemic inflammation. In neurodegeneration (n = 1), peripheral stimuli caused epigenetic reprogramming in microglia, yielding hyperresponsive or tolerized states modulating amyloid-β pathology. Convergent mechanisms (H3K4me3, glycolysis, mTOR/AhR/NLRP3) highlight trained immunity as a shared driver of chronic sterile inflammation.ConclusionsTrained immunity emerges as a unifying maladaptive mechanism perpetuating low-grade inflammation across these diseases, bridging transient endogenous insults to sustained pathology. Targeting reprogramming pathways, such as glycolysis or epigenetic inhibitors, offers promising therapeutic strategies. Expanded human studies are needed to address preclinical dominance and data gaps, particularly in CKD and neurodegeneration, where evidence is preliminary.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"32 ","pages":"17534259261446050"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770557","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}

{"title":"Engineered neutrophil, an emerging immune therapeutic strategy.","authors":"Jingyi Wang, Teng Deng, Ruisi Chen, Lu Yang, Yan Teng, Junming Miao","doi":"10.1177/17534259251365803","DOIUrl":"10.1177/17534259251365803","url":null,"abstract":"<p><p>Neutrophils play a pivotal role in the host immune system, serving as the frontline defense against microbial infections. They eradicate pathogens through diverse mechanisms, encompassing degranulation, phagocytosis, and the release of reactive oxygen species. Moreover, they are acknowledged as crucial contributors to chronic inflammatory pathological processes, including conditions such as cancer and autoimmune diseases. An expanding body of research suggests that neutrophils, harnessing their innate immune characteristics, possess the potential to serve as carriers for therapeutic agents or be directly employed in disease treatment. This underscores their potential as a cell therapy platform for future applications. Consequently, we systematically investigate the potential applications of neutrophils in this review, with a primary emphasis on elucidating the research advancements in utilizing neutrophils, including those derived from stem cells, for therapeutic interventions in various diseases.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251365803"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12361729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873063","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}

{"title":"Preclinical development of the TLR4 antagonist FP12 as a drug lead targeting the HMGB1/MD-2/TLR4 axis in lethal influenza infection.","authors":"Kari Ann Shirey, Alessio Romerio, Mohammed Monsoor Shaik, David S Leake, Charys Palmer, Natalia Skupinska, Jules Paton, Grisha Pirianov, Jorge Cg Blanco, Stefanie N Vogel, Francesco Peri","doi":"10.1177/17534259241313201","DOIUrl":"10.1177/17534259241313201","url":null,"abstract":"<p><strong>Background: </strong>Acute Lung Injuries (ALI) are a severe consequence of influenza-induced cytokine storm that can cause respiratory failure and death. It has been demonstrated that Toll-like Receptor 4 (TLR4) is involved in cytokine storm and that TLR4^-/- mice are protected against ALI. Therefore, TLR4 is a prime target for protection against ALI. FP12 is a known TLR4 antagonist that reduces TLR4-dependent immune activation and it is a promising lead compound for the treatment of innate immunity related pathologies.</p><p><strong>Objectives: </strong>We present here the preclinical development of FP12 as an anti-inflammatory lead compound acting on influenza-induced ALI.</p><p><strong>Methods: </strong><i>In vitro:</i> We pre-treated THP-1 cells with FP12 (10 μM) for 0.5 h, then exposed to LPS (100 ng/ml) for 0 to 16 h. In some experiments, cells were simultaneously incubated with FP12 and LPS, or FP12 was added 30 min after LPS. Cytokine levels were measured by Western blot and ELISA assays. <i>In vivo:</i> WT C57BL/6J mice were infected with mouse-adapted influenza virus (PR8). Two days after infection, mice received either vehicle, FP7 (200 µg/mouse), or FP12 (200 µg/mouse) once daily (Day 2 to Day 6). Mice were monitored daily for survival for 14 days. Data were collected through histological staining, qRT-PCR, and ELISA assay.</p><p><strong>Results: </strong>FP12 treatment inhibited both LPS- and HMGB1-induced TLR4 intracellular pathways (MyD88 and TRIF) leading to significantly reduced levels of a variety of proinflammatory cytokines including Type I interferon (IFN-β), highlighting its effectiveness in controlling proinflammatory protein production and reducing inflammation. FP12 protected mice therapeutically from influenza virus-induced lethality and reduced both cytokine gene expression and High Mobility Group Box 1 (HMGB1) levels in the lungs as well as ALI.</p><p><strong>Conclusion: </strong>FP12 can antagonize TLR4 activation in vitro and protects mice from severe influenza infection, most likely by reducing the TLR4-dependent cytokine storm mediated by danger-associated molecular patterns (DAMPs).</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259241313201"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143541972","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}

{"title":"Mutation within the transmembrane domain of oxidized low-density lipoprotein receptor 1 influences oxidized low-density lipoprotein-induced signal transduction.","authors":"Zhen Ma, Ran Xu, Jing Lu, Xiong Huang, Hao Jia, Zhiwen Ding, Jie Yuan, Yunzeng Zou","doi":"10.1177/17534259251350447","DOIUrl":"10.1177/17534259251350447","url":null,"abstract":"<p><p>ObjectiveTo investigate the important active sites within the NTFs to affect the <i>in vitro</i> interaction of oxidized low-density lipoprotein (ox-LDL) with its receptor, OLR1.MethodsSimulation analysis online was performed to generate various OLR1 chimeras, truncation mutants, and site-specific mutations. They were transfected in COS-7 cells and subjected to ox-LDL stimulations to observe the different reactions. Immunoprecipitation-mass spectrometry (IP-MS) was performed to show what proteins combined with OLR1 mutants in reaction to ox-LDL. Lipid uptake in human monocytes (THP-1) originated foam cells overexpressing somatic mutant of OLR1 were also determined. Further studies focusing on these regions were conducted using truncation mutants and site-specific mutants such as G43A, V44A, L45A, C46A, and L47A.ResultsAmino acids within the TM were highly conserved, spanning amino acids 35 to 57. The induction of intracellular p-ERK1/2 in response to ox-LDL stimulation was highly promoted in Chimera 3 possessing the TM from OLR1 like OLR1/WT (<i>p</i> < 0.05). Sequence alignment revealed two conserved regions within the TM of OLR1, Leu45-Cys46-Leu47 and Val55-Leu56-Gly57. Western blot showed that most of the TM changes ablated ERK1/2 activation in response to ox-LDL stimulation (<i>p</i> < 0.05). One human somatic mutation at L45F revealed significantly lower p-ERK1/2 levels with enhanced intake of ox-LDL in THP-1-derived foam cells than the control cells (<i>p</i> < 0.05). L45A and C46A molecular complexes were identified. After ox-LDL stimulation, these underlined interactions with keratins, namely KRT2 and KRT6A.ConclusionThese findings emphasize the vital role of the TM in the interactions between OLR1 and ox-LDL and point to an exciting possibility that signal transduction induced by ox-LDL through its receptor OLR1 may involve complex interactions with cytoskeletal proteins.</p>","PeriodicalId":13676,"journal":{"name":"Innate Immunity","volume":"31 ","pages":"17534259251350447"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12174723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302004","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}