Journal of Immunology Research最新文献

{"title":"Immunotherapy for Leiomyosarcoma: Current Status and Perspectives.","authors":"Haoyue Qi, Hanxi Zhang, Qin Wang, Xiaolu Wang, Limei Min, Yingling Zhou, Baorui Liu, Rutian Li","doi":"10.1155/jimr/6614578","DOIUrl":"10.1155/jimr/6614578","url":null,"abstract":"<p><p>Leiomyosarcoma (LMS), one of the soft-tissue sarcomas (STSs), has a relatively higher risk of distant metastasis. This has resulted in current first-line treatments still failing to deliver satisfactory outcomes, and the current treatment of LMS remains controversial and challenging. Therefore, it is worth thinking about how to guide and decide on the direction of treatment for LMS. In this review, we analyzed the immune microenvironment, gene expression, and molecular landscape of LMS, hinting at future research directions and prospects for LMS. We also analyzed the classical immunotherapy led by immune checkpoint inhibitors (ICIs), individualized immunotherapy such as cell therapy, and gene editing technologies, which bring better effect mechanisms and survival benefits, as well as opportunities and challenges for large-scale clinical applications.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e6614578"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13157314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147864107","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":"Regulatory Effects of CD14⁺CD16⁺⁺Slan⁺ Monocytes on Classical Monocytes and T Lymphocytes in Response to Inflammatory and Phagocytic Stimuli.","authors":"Cristian A Anacona, Karen Álvarez, Gloria Vásquez, Mauricio Rojas","doi":"10.1155/jimr/3322498","DOIUrl":"10.1155/jimr/3322498","url":null,"abstract":"<p><strong>Background: </strong>CD14⁺CD16⁺⁺6-sulfo LacNAc (Slan)⁺ monocytes represent a specialized nonclassical subset with reported pro-inflammatory and regulatory features. However, their capacity to modulate classical monocytes and T lymphocytes under apoptotic and inflammatory conditions remains incompletely defined.</p><p><strong>Methods: </strong>We employed a coculture reconstitution model using flow cytometry-sorted CD14⁺CD16⁺⁺Slan⁺ monocytes and CD14⁺⁺CD16^-Slan^- classical monocytes at defined ratios. Cultures were stimulated with lipopolysaccharide (LPS) or K562-derived apoptotic bodies (ABs). Monocyte surface marker expression was evaluated by flow cytometry, and cytokine concentrations were quantified using multiplex bead-based assays. The impact of Slan⁺ monocytes on CD3⁺ T cell proliferation and cytokine production was assessed following monocyte-T cell coculture.</p><p><strong>Results: </strong>CD14⁺CD16⁺⁺Slan⁺ monocytes exhibited enhanced uptake of ABs and distinct phenotypic modulation upon stimulation. Increasing proportions of Slan⁺ cells induced higher HLA-DR and CCR5 expression on classical monocytes. LPS stimulation promoted TNF, IL-12, IL-6, and CCL2 production, whereas AB exposure favored IL-10 and IL-17 accumulation. In coculture assays, Slan⁺ monocytes reduced CD4⁺ and CD8⁺ T cell proliferation and altered T cell cytokine profiles in a stimulus-dependent manner.</p><p><strong>Conclusion: </strong>CD14⁺CD16⁺⁺Slan⁺ monocytes exert a dose- and context-dependent modulatory effect on classical monocytes and T lymphocytes in vitro, displaying both inflammatory and regulatory properties depending on the stimulus. These findings highlight their functional plasticity within the human monocyte compartment.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e3322498"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13581061/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662903","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":"P2Y₂ Receptor Controls TLR3-Induced Chemokine Production in Intestinal Epithelial Cells.","authors":"Abdoul Karim Ouattara, Fariborz Bahrami, Radu Adrian Turcitu, Filip Kukulski, Joanna Lecka, Julie Pelletier, Nicolly Espindola Gelsleichter, Tais Vidal, Jean Sévigny","doi":"10.1155/jimr/4814045","DOIUrl":"10.1155/jimr/4814045","url":null,"abstract":"<p><p>Toll-like receptors (TLRs) and P2 receptors are key regulators of innate immunity. During infection, pathogen-associated molecular patterns (PAMPs) activate TLRs, whereas extracellular nucleotides engage P2 receptors and influence inflammatory responses. Here, we show that polyinosinic:polycytidylic acid (poly[I:C])-activated TLR3 and P2Y₂ signalling functionally interact in intestinal epithelial cells (IECs) to regulate chemokine production. HT-29 cells were stimulated with PAMPs, including the TLR3 agonist poly(I:C), in the presence or absence of P2 receptor signalling inhibitors. CXCL8/IL-8 or CXCL10/IP-10 secretion was assessed by ELISA and mRNA expression by quantitative real-time PCR (RT-qPCR). Primary IECs from P2Y₂ knock-out (KO) and wild-type (WT) mice were also treated with poly(I:C), and CXCL1/KC secretion was measured. Poly(I:C) stimulation induced robust CXCL8/IL-8 and CXCL10/IP-10 release in HT-29 cells. This response was inhibited by nucleotide scavenging, P2 receptor blockade, and P2Y₂ targeting using either specific antagonists or siRNAs. P2Y₂ was the dominant receptor expressed, and its ligands ATP/UTP constitutively released by these cells amplified CXCL8/IL-8 production induced by a suboptimal concentration of poly(I:C), while alone they had no effect. In support of these findings, primary IECs from P2Y₂ KO mice secreted significantly less CXCL1/KC than WT controls. Altogether, extracellular nucleotide signalling regulates TLR3-induced chemokine release in IECs through P2Y₂ receptors.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e4814045"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527233/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148865397","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":"Single-Cell Analysis of Hepatic Non-Parenchymal Cells Reveals Endothelial Dysfunction and Altered Endothelial and B Cell Communication in Acute-on-Chronic Liver Failure.","authors":"Jie Jia, Yuehong Dong, Yu Zhao, Shaoyou Li, Tangwei Mou","doi":"10.1155/jimr/5421823","DOIUrl":"10.1155/jimr/5421823","url":null,"abstract":"<p><p>Acute-on-chronic liver failure (ACLF) is a fatal syndrome defined by hepatic decompensation and systemic inflammation, yet the underlying cellular networks remain elusive. Here, we established an ACLF mouse model recapitulating clinical hallmarks and performed single-cell RNA sequencing (scRNA-seq) on hepatic non-parenchymal cells (NPCs). We identified 30 cell clusters and observed profound spatial remodeling of NPCs driven by pro-inflammatory mediators. Endothelial cells (ECs) underwent a critical transition from homeostasis to dysfunction, marked by mitochondrial damage and activation of NF-κB and MAPK pathways. Ligand-receptor interactome analysis identified dysfunctional ECs as central hubs driving global network reconfiguration, primarily via the Lgals9-Ighm/Cd45/Cd44 axes, alongside the suppression of homeostatic signals (Cd55 and APP). Furthermore, we mapped B cell lineage trajectories and validated the spatial co-localization of EC and B-cell interactions through Lgals9-Ighm. This study defines the EC and B-cell communication landscape and suggests that the Lgals9-Ighm axis may play a critical role in ACLF progression, representing a potential candidate for therapeutic intervention.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e5421823"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13528445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148865457","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":"A Bead-Based Screening Platform for Identifying Monoclonal Antibodies That Disrupt PD-1/PD-L1 Interactions.","authors":"Veridiane M Pscheidt, Rodrigo B Gassen, José E Sacconi Nunes, Deise do Nascimento de Freitas, Valdir Barth, Fernanda B Frozza, Milena D Santos, Claudia P Nunes, Cristina B C Bonorino","doi":"10.1155/jimr/5189659","DOIUrl":"10.1155/jimr/5189659","url":null,"abstract":"<p><p>Monoclonal antibodies (mAbs) targeting immune checkpoint pathways such as programmed cell death protein 1 (PD-1)/PD-L1 are central to modern immunotherapy, yet scalable methods to assess their functional blockade remain limited. We present a bead-based flow cytometry assay for quantifying the inhibition of PD-1/PD-L1 interaction by antibodies. Recombinant human PD-1 protein was conjugated to polystyrene beads, and its interaction with recombinant human PD-L1 protein labeled with a fluorochrome was measured. The inhibitory activity of an anti-PD-L1 mAb was quantified based on their ability to disrupt this interaction. The assay was validated for intra- and inter-assay precision, in addition, functionality was confirmed using a T cell coculture assay. The assay demonstrated dose-dependent inhibition by the αPD-L1 mAb, with a calculated mean IC₅₀ of 3.122 µg/mL. The method proved to be reproducible for the determination of antibody blocking activity, with relative standard deviation (RSD) < 20% between three independent runs. At the concentration approximating the IC₅₀ detected on the bead assay, the antibody significantly restored CD69 expression on the T cell surface (p = 0.0001) in a coculture in vitro system. In addition, the methodology could successfully distinguish the blocking capacity of two anti-PD-L1 antibodies with different affinities. This high-throughput compatible platform offers a reliable tool for screening PD-1/PD-L1 blocking antibodies, supporting immunotherapy discovery and development.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e5189659"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581428","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":"Associations Between Immune Senescence and Immune Reconstitution Among People Living With HIV Undergoing Antiretroviral Therapy.","authors":"Zhe Qian, Huolan Long, Houji Wu, Jingfang Xie, Suling Chen, Jian Wu, Shaohang Cai","doi":"10.1155/jimr/8683624","DOIUrl":"10.1155/jimr/8683624","url":null,"abstract":"<p><strong>Background: </strong>Failure of immune reconstitution (IR), characterized by suboptimal CD4⁺ T-cell recovery despite virologic suppression on antiretroviral therapy (ART), remains a critical challenge for people living with human immunodeficiency virus (PLWHIV). The contribution of immune senescence to this failure is incompletely understood.</p><p><strong>Objective: </strong>This study aimed to determine the role of pre-ART immune senescence characterized by lymphocyte profile and lymphocyte cellular senescence markers in nonimmune reconstitution (NIR) after 48 weeks of ART initiation.</p><p><strong>Methods: </strong>We first performed a SenMayo gene set score from publicly available CD4⁺ T-cell scRNA-seq data. Subsequently, a prospective cohort of 510 ART-initiating PLWHIV was assessed at baseline and week 48. IR was strictly defined as a CD4⁺ T-cell count increase over 350 cells/uL. Logistic regression; immunophenotyping; cytokine profiling, including TNF-α, IFN-γ and CD-107a; and cellular senescence marker, including p16, p21, p53, and senescence-associated β-galactosidase assessments identified NIR factors.</p><p><strong>Results: </strong>Bioinformatics analysis revealed multiple ART-naïve CD4⁺ T-cell subtypes exhibited elevated cellular senescence scores. Patients with IR were significantly younger than those with NIR (both in AIDS and non-AIDS subcohorts, p  < 0.05). Multivariable analysis indicated age was an independent risk factor for NIR. Before ART initiation, the NIR group exhibited a distinctly senescent immune profile characterized by reduced naïve T cells, increased terminally differentiated T cells, and heightened chronic inflammation with elevated cytokine secretion. ART failed to fully reverse these immune abnormalities, and cellular senescence was most pronounced in CD4⁺ T cells within the NIR group prior to treatment.</p><p><strong>Conclusion: </strong>Pre-ART immune senescence is strongly associated with NIR in PLWHIV receiving ART. These findings necessitate considering immunological age and immune senescent status for personalized therapeutic strategies.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e8683624"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13239133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148143743","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":"Associations Between Short-Term Changes in Disease Activity and Long-Term Clinical Outcomes in Activated Phosphoinositide 3-Kinase Delta Syndrome.","authors":"Joanne Tutein Nolthenius, Barbara Torlinska, Louise Linsell, Neil Hawkins, Yuxian Chen, John Whalen, Anna Šedivá","doi":"10.1155/jimr/1486611","DOIUrl":"10.1155/jimr/1486611","url":null,"abstract":"<p><strong>Background: </strong>Clinical trials in activated phosphoinositide 3-kinase delta (PI3Kδ) syndrome (APDS), an ultra-rare disease, have evaluated treatment response to the PI3Kδ inhibitor leniolisib using disease activity endpoints, including those measuring immunodeficiency and immune dysregulation. However, the relationship between disease activity endpoints and long-term clinical outcomes has not been quantified.</p><p><strong>Methods: </strong>Data from a randomised controlled trial and its open-label extension (OLE) investigating leniolisib were used to evaluate associations between short-term disease activity endpoints and longer-term clinical outcomes. Both single time point and repeated measures analyses were conducted using linear regression modelling and random effects multilevel regression modelling, respectively.</p><p><strong>Results: </strong>In total, 39 patients were included (≤6 years of follow-up). Improvements in multiple immunodeficiency and dysregulation disease activity endpoints were significantly associated with increases in the patient global assessment (PtGA) and the 36-item short form survey (SF-36) physical component score and mental component score (PCS/MCS). Increasing proportion of naïve B cells was associated with reduction in infection rates (2.3% fewer infections per 1% increase in naïve B cells).</p><p><strong>Conclusions: </strong>In this clinical trial setting, short-term improvements in immunodeficiency and dysregulation following treatment with leniolisib were associated with longer-term improvements in clinical outcomes, including infection rates and quality of life, for patients with APDS.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1486611"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13583054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982657","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":"Targeted Clearance of Senescent Endothelium by GPNMB-Specific CAR-T Cells.","authors":"Peijie Yu, Jie Du, Yan Liu, Mei Zhou","doi":"10.1155/jimr/1976386","DOIUrl":"10.1155/jimr/1976386","url":null,"abstract":"<p><p>Endothelial cells (ECs) serve as crucial components of blood vessels and are vital for preserving vascular health in humans. The aging of these cells significantly accelerates vascular aging. Factors released by aging ECs serve as key initiators of arterial dysfunction and various cardiometabolic diseases. As a result, the targeted removal of aging ECs from injured tissues could reduce these issues and potentially improve lifespan. In this research, we explored the therapeutic capabilities of chimeric antigen receptor (CAR)-T cells designed to focus on senescent cells as potential senolytic agents. We identified GPNMB, a transmembrane glycoprotein, as a protein characterized by extensive expression during cellular senescence. Our findings demonstrate that CAR-T cells specifically targeting GPNMB can efficiently remove senescent cells in vitro. In addition to this, the engineered CAR-T cells significantly clear replicative and doxorubicin (Dox)-induced senescent human umbilical vein ECs (HUVECs). Notably, these CAR-T cells successfully eradicated senescent HUVECs within a Matrigel matrix implanted subcutaneously in mice, thereby creating a simulated in vivo environment that mimics physiological conditions. The findings emphasize the possibilities of CAR-T cells in treating EC senescence.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1976386"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439632/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148673817","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 Role of m6A Modification in the Development of Systemic Lupus Erythematosus via the TGF-β Signaling Pathway.","authors":"Xin Xia, Rui Qu","doi":"10.1155/jimr/7142984","DOIUrl":"10.1155/jimr/7142984","url":null,"abstract":"<p><p>N6-methyladenosine (m6A) modification is the most widespread RNA internal modification involved in RNA metabolism, participating in cell biology and immune responses. In the early stage of systemic lupus erythematosus (SLE), m6A modification can affect the production of autoantibodies by regulating the differentiation of T follicular helper (Tfh) cells and the generation of autoreactive B cells. With the development of SLE, its subsequent action in immune complexes (ICs)-deposited tissues is the promotion of excessive fibrosis, causing progressive organ damage. TGF-β is the central driver activating fibroblasts, inducing epithelial-to-mesenchymal transition (EMT), and promoting extensive extracellular matrix (ECM) deposition via the SMAD pathway, ultimately leading to tissue fibrosis and organ damage. m6A regulators can act on both upstream and downstream components of the TGF-β signaling pathway. They can synergize with TGF-β transcription factors to control the amplification of TGF-β signaling. Furthermore, they can work with target molecules downstream of the TGF-β receptor (TGF-βR) to tune TGF-β/SMAD pathway activity, increasing the expression of profibrotic transcripts. It is suggested that inhibition of m6A modification targeting the TGF-β signaling pathway can effectively reduce EMT and fibrosis in multiple organs, especially in the kidney, improving the long-term prognosis of SLE patients. In this review, we focus on the role of TGF-β in the pathogenesis of SLE, the mechanism by which m6A modifications affect the TGF-β signaling pathway, and its impact on EMT and fibrosis in different organs, trying to provide a new treatment strategy for the control of SLE symptoms.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e7142984"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074660","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":"Aspergillus fumigatus Gliotoxin Inhibits LC3-Associated Phagocytosis in Macrophages in a Calcium-Dependent Manner.","authors":"Yuqing Sun, Fangyan Chen, Ling Zhang, Caopei Zheng, Yu Wang, Yulin Zhang, Li Han","doi":"10.1155/jimr/5542735","DOIUrl":"10.1155/jimr/5542735","url":null,"abstract":"<p><p>As a pivotal secondary metabolite of Aspergillus fumigatus, gliotoxin (GT) has many toxicological effects on mammalian cells; however, its function on LC3-associated phagocytosis (LAP) induced by A. fumigatus in macrophages is poorly understood. Here, it was found that pretreatment of macrophages with GT can significantly attenuate the conversion of LC3-II. In parallel, the expression of Rubicon, the putative indicator of LAP in macrophages, was dampened in a similar trend. Loss of ability to produce GT made the conidia of gliPΔ mutant of A. fumigatus induce more LC3-II conversion in THP1 cells, which could be inhibited by exogenous GT. Comparative transcriptomic analysis showed that GT can promote the expression of MAPK10, and the calcium-release regulatory pathway was enriched between the differentially expressed genes. Further, GT promotes the release of ROS at a concentration of 50 ng/mL, and inhibition by GT on LC3-II production in macrophages during A. fumigatus infection could be restored by pretreatment with calcium inhibitors but not affected by the inhibitors for JNK and siRNA for MAKP10. Collectively, our data demonstrated that GT exerts an inhibitory effect on LC3-associated phagocytosis in macrophages via a calcium-dependent mechanism, and MAPK10 exists downstream of LAP.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e5542735"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13128990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773433","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}