MOLECULAR IMMUNOLOGY分子免疫学
MOLECULAR IMMUNOLOGY(英文缩写 MOL IMMUNOL),ISSN 0161-5890,eISSN 1872-9142,中文译名:分子免疫学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 4.174 | Q3 |
| 2022 | 3.600 | Q3 |
| 2023 | 3.200 | Q2 |
| 2024 | 3.000 | Q3 |
| 2025 | 3.700 | Q2 |
MOLECULAR IMMUNOLOGY 最新收录文献
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1. Pristimerin suppresses the phenotypic switch of vascular smooth muscle cells in atherosclerosis through inhibiting the activation of JAK2/STAT3 pathway.
PMID:日期:2026-10-01The aim of our research was to investigate the potential effect of pristimerin (Pris) on atherosclerosis (AS), and clarify its underlying molecular mechanisms. The effect of Pris on atherosclerotic lesions were assessed by using HE staining and Oil red O staining. Moreover, serum lipid profiles also detected using the commercial reagent kits. Inflammatory factors expression was determined employing qRT-PCR. The proteins associated with the phenotypic transformation of VSMCs and JAK2/STAT3 pathway-related proteins were assessed using western blot, immunohistochemistry and immunofluorescence. The proliferation and migration of VSMCs were determined utilizing EdU and Transwell assay. We found that Pris could suppress atherosclerotic lesions in mice. Moreover, Pris ameliorated lipid metabolism disorders and inflammation, and inhibited the phenotypic transformation of VSMCs in mice. In ox-LDL-treated VSMCs, Pris could also inhibit the phenotypic transformation and inflammatory responses. Subsequently, Pris was demonstrated to inhibit JAK2/STAT3 pathway in both HFD-caused AS mice and ox-LDL-treated VSMCs. The inhibition of Pris on the phenotypic transformation and inflammatory responses in VSMCs could be reversed by Colivelin TFA. Pris could alleviate the progression of AS by inhibiting the phenotypic transformation of VSMCs and inflammatory responses via suppressing the activation of JAK2/STAT3 pathway.
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2. PD-L1 upregulated by IGF1R via the PI3K/AKT/NF-κB axis induces sorafenib resistance in hepatocellular carcinoma.
PMID:日期:2026-10-01Aberrant activation of insulin-like growth factor 1 receptor (IGF1R) in hepatocellular carcinoma (HCC) is closely associated with resistance to targeted therapies. However, the mechanism by which IGF1R transcriptionally upregulates programmed death-ligand 1 (PD-L1) to drive sorafenib resistance remained unclear. This study aimed to elucidate the molecular pathway through which IGF1R upregulates PD-L1 via the PI3K/AKT/NF-κB signaling cascade, thereby promoting sorafenib resistance. The regulatory network of the IGF1R-PI3K/AKT/NF-κB-PD-L1 axis was analyzed using immunohistochemistry (20 HCC clinical samples), Western blotting (THLE-2 and Huh7/Hep3B/SNU-387 cells), functional assays (CCK8, colony formation, Transwell, JC-1, Annexin V-FITC/PI), chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays. Two independent in vivo cohorts were established: Cohort 1(SCID mice bearing Huh7 xenografts, IGF1 + sorafenib (SFB)) to assess IGF1R-driven resistance; Cohort 2 (NOD-SCID mice/SNU-387, PD-L1 knockdown/overexpression ± sorafenib) to validate PD-L1 as the downstream effector. IGF1R was significantly overexpressed in HCC. IGF1R activation increased the sorafenib IC by 2.3-fold and activated PI3K/AKT/NF-κB signaling. NF-κB directly bound to the PD-L1 promoter to drive its transcription, as confirmed by ChIP and dual-luciferase assays. PI3K inhibition with LY294002 blocked IGF1R-induced PD-L1 upregulation and restored sorafenib sensitivity. PD-L1 overexpression promoted HCC proliferation, migration, and cell-cycle progression while suppressing apoptosis; PD-L1 knockdown yielded opposite effects. In vivo, Cohort 1 confirmed that IGF1R activation promoted tumor growth, attenuated sorafenib efficacy, and elevated p-AKT, p-NF-κB, and PD-L1 in tumor tissues. Cohort 2 demonstrated that PD-L1 knockdown augmented sorafenib-induced tumor suppression, whereas PD-L1 overexpression blunted sorafenib efficacy, with reciprocal changes in Ki-67 and pathway phosphorylation. IGF1R upregulates PD-L1 via the PI3K/AKT/NF-κB axis through direct NF-κB-mediated transcriptional activation, and PD-L1 serves as a critical downstream effector driving sorafenib resistance in HCC.
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3. Preliminary exploration of effects of the JAK inhibitor tofacitinib on pyoderma gangrenosum: In vitro inhibition of NETs and Th17 differentiation.
PMID:日期:2026-10-01Pyoderma gangrenosum (PG), a refractory inflammatory disorder, remains a condition with incompletely understood pathogenesis. Currently, no FDA-approved treatments are available. Janus kinase (JAK) inhibitors have been reported sporadically in case studies as effective treatments for PG. To characterize the cellular and molecular landscape associated with JAK/STAT (signal transducer and activator of transcription) pathway overactivation in PG lesions, and investigate the potential effects of tofacitinib on PG. Single-cell RNA sequencing (scRNA-seq) and multiplex immunohistochemistry (mIHC) were employed to characterize the cellular and molecular landscape of JAK/STAT pathway overactivation in PG. In vitro experiments (immunostaining, qPCR, western blot, flow cytometry) were performed to further validate the potential effects of tofacitinib on PG. We identified significant overactivation of the JAK/STAT pathway in PG lesions-particularly in advanced stages-which, in terms of immune inflammation, is primarily driven by myeloid cells and T cells. This activation was associated with enhanced neutrophil extracellular trap (NET) formation in myeloid cells and aberrant differentiation/plasticity of Th17 and Th17.1 (IL-17/IFN-γ double-producing) cells. In vitro cell experiments further demonstrated that the JAK inhibitor tofacitinib suppresses STAT phosphorylation in myeloid and T cells, myeloid NETosis, and IL-17A production. Our study investigated immunological profiling of PG lesions via scRNA-seq and mIHC, along with in vitro validation. These findings delineate a multi-axis cellular and molecular landscape of PG linked to aberrant JAK/STAT signaling, and provide preliminary in vitro evidence supporting potential inhibitory effects of tofacitinib on key pathological processes of PG.
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4. Exploring the relationship between natural and cryptic polyreactivity in human antibodies.
PMID:日期:2026-10-01Antibody polyreactivity, defined as the ability of a single antibody molecule to recognize multiple unrelated antigens, is a common feature of the human antibody repertoire and contributes to immune defense and homeostasis. In addition to naturally occurring polyreactivity, antibodies can acquire inducible polyreactivity following exposure to environmental factors such as heme, ferrous ions, reactive oxygen species, or protein-destabilizing conditions. Although this "cryptic" polyreactivity is thought to arise in inflammatory and hemolytic settings, its relationship with natural polyreactivity remains poorly understood. In this commentary, we examine whether cryptic polyreactivity represents an amplification of pre-existing antigen-binding promiscuity or instead emerges de novo in otherwise monospecific antibodies. Analyses of clinical-stage therapeutic antibody repertoires indicate that heme- or ferrous ion-induced polyreactivity does not correlate with baseline natural polyreactivity, suggesting that these phenomena are largely mechanistically distinct. However, heme can enhance the promiscuous antigen recognition of certain naturally polyreactive broadly neutralizing anti-HIV-1 antibodies, underscoring the complexity of this phenomenon. A better understanding of the relationship between natural and cryptic antibody polyreactivity may help identify hidden liabilities in therapeutic antibodies and provide new insight into the adaptive flexibility of humoral immunity.
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5. Artemisinin ameliorates experimental autoimmune prostatitis by suppressing NLRP3 inflammasome-induced pyroptosis via the Nrf2/HO-1 axis.
PMID:日期:2026-10-01Chronic prostatitis (CP) is common in young males. The etiology is unclear and treatment options are limited. Pyroptosis, a newly identified type of cell death, has been linked to CP pathogenesis, warranting further investigation. Here, the therapeutic effects of artemisinin (ART) on chronic non-specific inflammation were assessed. Comprehensive analyses, including evaluation of chronic pain progression, histopathology, and cytokine levels, revealed that ART significantly and dose-dependently suppressed NOD-like receptor protein 3 (NLRP3) inflammasome-mediated pyroptosis and alleviated pathological damage in experimental autoimmune prostatitis. Mechanistic studies indicated that ART markedly reduced oxidative stress in autoimmune mouse models by stimulating the Nrf2/HO-1 axis. The effects of ART were blocked by a specific Nrf2/HO-1 inhibitor, preventing inflammasome-mediated induction of pyroptosis. Cellular experiments showed that ART elevated Nrf2 levels and suppressed NLRP3 inflammasome-mediated pyroptosis in RAW264.7 macrophages following lipopolysaccharide (LPS) stimulation. In summary, ART mitigates CP by modulating the Nrf2/HO-1 pathway, thereby reducing oxidative stress and suppressing NLRP3-inflammasome-induced pyroptosis.
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6. STK39 interacts with MAPK14 to facilitate cardiomyocyte pyroptosis in septic cardiomyopathy by inducing NLRP3 inflammasome.
6. STK39与MAPK14相互作用，通过诱导NLRP3炎性小体促进感染性心肌病中的心肌细胞焦亡PMID:日期:2026-10-01Septic cardiomyopathy (SCM) is a severe manifestation of sepsis characterized by myocardial dysfunction and systemic inflammation. The NLRP3 inflammasome-driven pyroptosis plays a pivotal role in SCM pathogenesis. This study aimed to elucidate the upstream molecular regulators of pyroptosis in SCM and investigate the functional role of serine/threonine kinase 39 (STK39) in modulating NLRP3 inflammasome activation. Peripheral blood samples were collected from 44 patients with sepsis (19 with SCM) and 30 healthy controls. A murine cecal ligation and puncture (CLP) model and LPS-stimulated human cardiomyocytes (HCMs) were employed to simulate SCM. Cardiac function was assessed via echocardiography, and pyroptosis markers were quantified using ELISA, qRT-PCR, and western blot. Protein interactions and transcriptional regulation were evaluated by co-immunoprecipitation (Co-IP), chromatin immunoprecipitation (ChIP), immunofluorescence, and dual-luciferase reporter assays. STK39 expression was upregulated in SCM patients and septic mice. STK39 knockdown significantly attenuated cardiac pyroptosis in LPS-treated HCMs, and improved myocardial function in CLP-induced mice. Mechanistically, STK39 interacted with MAPK14 to activate p38 MAPK signaling, promoting ELK1-mediated transcriptional upregulation of NLRP3 and subsequent pyroptotic cell death. Rescue assay demonstrated that activation of p38 MAPK signaling greatly diminished the protective roles of STK39 silence on cardiomyocyte pyroptosis. This study identifies STK39 as a novel upstream regulator of NLRP3 inflammasome-mediated pyroptosis in SCM through the MAPK14/ELK1 signaling axis. These findings suggest that STK39 may serve as a potential molecular target for SCM.
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7. iPSC-derived polyvalent vaccines as ontogenetically informed immunogens toward overcoming immune refractoriness in microsatellite-stable colorectal cancer: An emerging frontier in cancer immunotherapy.
7. iPSC-衍生的多价疫苗作为个体遗传知情免疫原，用于克服可微卫星结直肠癌癌症中的免疫难治性：癌症免疫疗法的一个新兴前沿PMID:日期:2026-10-01Colorectal carcinoma (CRC) exerts a growing global disease burden, with microsatellite-stable/proficient mismatch repair (MSS/pMMR) tumors exhibiting intrinsic refractoriness to immune-checkpoint blockade (ICB) owing to low tumor mutational burden, limited neoantigenicity, and an immunosuppressive tumor microenvironment (TME) dominated by regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs). This review synthesizes evidence on induced pluripotent stem cell (iPSC)-derived polyvalent vaccines as ontogenetically recapitulative immunogens, evaluating their mechanistic basis, preclinical efficacy across cancer models, and translational prospects in MSS CRC. Reprogramming induces re-expression of oncofetal tumor-associated antigens, including cancer-testis antigens (NY-ESO-1, MAGE-A3) and aberrant glycoforms of CEA and MUC1, that are natively shared between iPSCs and CRC cells. Clinically actionable neoepitopes such as KRAS^G12D/V are not a consequence of reprogramming itself but can be introduced into iPSCs by deliberate genetic engineering (neoantigen-augmented iPSCs), complementing this native oncofetal repertoire and broadening the antigenic payload available for epitope spreading following vaccine-induced tumor cell death. Irradiated autologous or syngeneic iPSCs, delivered with TLR9 agonists, drive CD8⁺ cytotoxic T-cell activation, Th1 polarization, perforin/granzyme-mediated cytolysis, and favorable effector-to-suppressor ratios. Preclinical models of melanoma, pancreatic ductal adenocarcinoma, and MSS CRC demonstrate prophylactic and therapeutic efficacy, with neoantigen-enhanced iPSCs synergizing with radiotherapy-induced DAMPs to achieve durable regressions and memory T-cell formation. Translational priorities include CRISPR-engineered hypoimmunogenic iPSC platforms, GMP-compatible non-integrating reprogramming, and combinatorial integration with STING agonists, ICB, CAR-NK cells, and LNP-mRNA constructs to enable biomarker-guided clinical deployment in minimal-residual-disease CRC.
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8. Guchang capsule alleviates inflammatory bowel disease by downregulating lncRNA THRIL and inhibiting the p38 MAPK/NF-κB signaling pathway.
PMID:日期:2026-10-01Inflammatory bowel disease (IBD) is a chronic inflammatory disorder with limited treatment options. Guchang capsule (GC) has been used in traditional Chinese medicine, but its effects on IBD and the underlying molecular mechanisms remain unclear. A dextran sulfate sodium (DSS)-induced colitis model in mice and an H₂O₂-induced Caco-2 cell injury model were established. Network pharmacology, Transwell co-culture, lncRNA THRIL overexpression/knockdown, and pathway intervention approaches were employed to systematically investigate the mechanism of GC in IBD. GC attenuated colonic inflammation and tissue damage in vivo, suppressed pro-inflammatory cytokines while restoring anti-inflammatory cytokines, and exhibited a dose-dependent protective effect on Caco-2 cells in vitro. Network pharmacology suggested that the p38 MAPK and NF-κB pathways might serve as key candidate pathways of GC. Mechanistically, p38 MAPK appeared to act upstream of NF-κB, and GC showed inhibitory effects on the activation of both pathways. In the intestinal epithelial-macrophage co-culture system, GC tended to restore barrier function and promote M1-to-M2 macrophage polarization. GC downregulated THRIL expression both in vivo and in vitro. THRIL overexpression activated p38 MAPK and NF-κB and partially attenuated the protective effects of GC, while THRIL knockdown partially mimicked the anti-inflammatory action of GC and exhibited a certain synergistic tendency. GC may alleviate DSS-induced colitis by downregulating THRIL and inhibiting the p38 MAPK and NF-κB pathways, providing a molecular basis for its therapeutic application in inflammatory bowel disease.
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9. Colchicine attenuates cardiac hypertrophy by targeting the macrophage-driven Interleukin-6 suppression.
PMID:日期:2026-10-01Hypertrophic cardiomyopathy (HCM), the most prevalent inherited cardiovascular disease, is strongly linked to progressive heart failure and sudden cardiac death (SCD). However, its underlying pathogenic mechanisms remain incompletely understood, and effective therapeutic strategies are still lacking. Here, we established two murine HCM models harboring high SCD risk-associated mutations. Single-cell RNA sequencing revealed immune activation and enhanced fibrotic remodeling in the myocardium of these models. Therefore, we hypothesized that colchicine, a widely used anti-inflammatory drug known to reduce cardiovascular events in multiple cardiac disorders, may also represent a promising therapeutic candidate for HCM. As we expected, colchicine treatment attenuated pathological remodeling in our study, as evidenced by reduced cardiomyocyte hypertrophy, decreased fibrosis, and downregulation of cardiac stress markers (Anp, Bnp) and fibrotic mediators (Ctgf, Col1a1, Col3a1). In addition, colchicine attenuated pro-inflammatory macrophage populations and suppressed IL-6 expression, thereby contributing to the preservation of cardiac function. These findings provide the first preclinical evidence that colchicine alleviates myocardial inflammation and fibrosis in HCM, underscoring its potential as a novel therapeutic strategy to reduce fibrosis, lower SCD risk, and improve patient outcomes.
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10. Gut microbiota-derived lactate alleviates intestinal ischemia-reperfusion injury by suppressing macrophage M1 polarization via the NF-κB pathway.
PMID:日期:2026-10-01Intestinal ischemia-reperfusion (I/R) injury is a critical clinical condition whose pathogenesis is closely associated with immune-inflammatory responses. In this process, macrophage polarization plays a pivotal role in the initiation and progression of inflammation. While lactate, a microbial metabolite, has been shown to exert significant immunomodulatory effects and can influence macrophage polarization. Therefore, this study aimed to investigate the function of lactate and macrophage polarization in I/R injury. This study aimed to investigate whether gut microbiota-derived lactate regulates macrophage M1 polarization via the NF-κB signaling pathway, thereby mitigating intestinal I/R injury. A rat model of intestinal I/R injury was established. A time gradient of reperfusion was set to determine the optimal time point for observation. Interventions including macrophage depletion, antibiotic treatment, lactate administration, and NF-κB inhibition were employed. Intestinal injury severity, macrophage polarization status, and NF-κB pathway activity were analyzed using histopathology, immunofluorescence, Western blot, and qPCR. For in vitro experiments, macrophages were treated with LPS and/or lactate, with polarization phenotypes assessed by flow cytometry and immunofluorescence. Comparative analysis of Sham, I/R, and macrophage-depleted (I/R+MPD) groups revealed an increased proportion of M1 macrophages following I/R, while macrophage depletion attenuated intestinal injury, demonstrating the involvement of M1 polarization in I/R pathology. Time-course analysis demonstrated that the proportion of M1 macrophages peaked at 2-6 h of reperfusion, whereas intestinal lactate content reached its minimum at 2 h after reperfusion. Comparison among Sham, I/R, and antibiotic-treated (I/R+ABX) groups showed that gut microbiota depletion exacerbated intestinal injury and increased M1 macrophage proportion, indicating a protective role of gut microbiota against I/R injury. Furthermore, in vitro lactate treatment reduced M1 polarization in RAW264.7 cells. In vivo lactate administration alleviated intestinal tissue damage and decreased serum levels of pro-inflammatory cytokines secreted by M1 macrophages. Finally, Western blot analysis confirmed that lactate treatment suppressed phosphorylation of NF-κB pathway proteins p65 and IκBα. The gut microbiota metabolite lactate may alleviate intestinal I/R injury by inhibiting the NF-κB pathway and reducing macrophage M1 polarization.