HUMAN IMMUNOLOGY人类免疫学
HUMAN IMMUNOLOGY(英文缩写 HUM IMMUNOL),ISSN 0198-8859,eISSN 1879-1166,中文译名:人类免疫学 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：2025-10-01 至 2026-09-30，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 | 2.211 | Q4 |
| 2022 | 2.700 | Q4 |
| 2023 | 3.100 | Q3 |
| 2024 | 2.200 | Q3 |
| 2025 | 2.100 | Q4 |
HUMAN IMMUNOLOGY 最新收录文献
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1. Genome-wide transcriptomics and a machine learning-based random forest model identify novel biomarkers to predict phenotypic variability in Wilson disease.
PMID:日期:2026-10-02Genotype-phenotype correlation studies fail to explain the phenotypic diversity in Wilson disease (WD) and the missing link may lie in transcriptomics. Therefore, we performed genome-wide transcriptomic profiling and machine-learning-based random forest modeling (RF) to identify the most important genes that could explain phenotypic variability in WD and reveal the molecular pathogenesis of WD. For this purpose, we used bulk RNA sequencing approaches to include 47 genetically confirmed pediatric hepatic WD patients and controls. We observed 321 differentially expressed genes (DEGs) in WD. Among top 100 DEGs, 42 significant DEGs (p < 0.05) were correlated with Kayser-Fleischer ring, serum ceruloplasmin, 24-h urinary copper levels, PELD score at recruitment, and degree of presentation at diagnosis. The random forest model identified a panel of ten genes: GPR37L1, OIP5, TRAJ23, IGHA2, TDRD1, LILRA4, HMOX2, UGT2B17, IGLV7-46 and EPHA1 that could explain 97.22% of phenotypic variability in WD. Ingenuity pathway analysis ranked MAP kinase pathway highest, driven by upregulation of RPS6KA1 (logFC = 4.68) and downregulation of DUSP16 (logFC = -5.22), and GAPLINC (logFC = -2.45). Iron homeostasis signaling demonstrated comparable enrichment, involving key genes ATP6V0D2 (logFC = -4.06), HMOX2 (logFC = -2.70), HBD (logFC = 1.96) and HBZ (logFC = 1.76). These results suggest that children with WD have dysregulation in MAP Kinase and iron homeostasis signaling pathways providing an important insight into the molecular pathogenesis of WD. RF modeling identified a panel of biomarker with ten genes, that could explain the phenotypic variability in WD.
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2. Rational truncation of streptokinase reduces immunogenicity while preserving plasminogen activation: in vitro and in vivo analysis.
PMID:日期:2026-09-29The clinical utility of streptokinase, a widely used and cost-effective thrombolytic agent, has gained importance post COVID-19 due to increase in cardiovascular diseases globally. But the strong humoral immunogenicity exhibited by it, restricts its usage. Building upon our prior work of developing truncated streptokinase variants and their plasminogen activation study, we report here the results of immunogenicity studies for identification of variants with reduced immunogenicity. A panel of ten rationally truncated and recombinantly expressed streptokinase fragments were screened for antibody recognition and immunogenicity potential. Out of the ten fragments, two N-terminal constructs (amino acid residues 1-300 and 1-173) exhibited approximately 40-45% lower ELISA immunoreactivity compared with full-length streptokinase during initial in vitro screening. These fragments were also already reported to retain >85% of native plasminogen activation activity. In vivo evaluation of the fragments in rabbits demonstrated significantly attenuated humoral responses over a 28-day immunization period, confirmed by longitudinal antibody titration and cumulative area-under-the-curve analysis when compared to the full-length streptokinase. Fragment 1-173 emerged as a promising lower-immunogenic thrombolytic candidate, and this work demonstrates that rational domain minimization can decouple functional competence from immunodominant regions in streptokinase establishing a broadly applicable framework for engineering improved therapeutic proteins.
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3. Poly(I:C) stimulation upregulates HLA-G expression in human nasal epithelial cells.
PMID:日期:2026-09-29Human leukocyte antigen (HLA)-G is an immunosuppressive molecule involved in inflammation and has been reported to be induced by viral infections. Although the upper airway is a major entry site for viral pathogens, the expression of HLA-G in the nasal mucosa and its regulatory mechanisms remain unclear. We investigated HLA-G expression in primary human nasal epithelial cells (HNECs) and whether it is regulated by Toll-like receptor (TLR) stimulation. HNECs were stimulated with TLR1-9 agonists. HLA-G mRNA expression was quantified by reverse transcription quantitative polymerase chain reaction (RT-qPCR), and HLA-G protein expression was assessed by Western blotting. HLA-G mRNA was detected in unstimulated HNECs. Among the TLR agonists tested, TLR3 (polyinosinic-polycytidylic acid [Poly(I:C)]) stimulation significantly upregulated HLA-G mRNA expression (2.85-fold, 95% confidence interval 1.98-4.10). HLA-G mRNA expression increased with Poly(I:C) concentration, with significant upregulation at 1 and 10 μg/mL and a significant dose-response trend. At 10 μg/mL, mRNA expression was significantly upregulated from 16 h onward. Western blotting revealed that Poly(I:C) stimulation significantly upregulated HLA-G protein expression. These findings demonstrate HLA-G expression in HNECs and its upregulation by Poly(I:C), suggesting that HLA-G may be regulated in response to dsRNA-triggered innate immune signaling in the nasal epithelium.
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4. Mapping immune cell metabolic reprogramming from mechanistic hotspots to translational directions: A bibliometric analysis with exploratory clinical evidence.
PMID:日期:2026-09-26Immune cell metabolic reprogramming links immune function, disease microenvironments, and therapeutic responses. Although research in this field has expanded rapidly, the relationships among immune cell types, metabolic pathways, and clinical scenarios remain fragmented. English language articles and reviews published from 2008 to 2025 were retrieved from the Web of Science Core Collection on June 14, 2025, and 3137 records were finally included. Bibliometrix, CiteSpace, VOSviewer, and related visualization tools were used for bibliometric and visual analyses. In addition, a PubMed clinical subset was established by retrieving human clinical studies published between January 1, 2008 and August 26, 2025. A total of 11 clinical studies were included. The results showed that research on immune cell metabolic reprogramming entered a phase of rapid growth after 2016, with China and the United States as the leading contributing countries. The knowledge base of the field was mainly centered on T cell metabolic regulation, macrophage function, the tumor microenvironment, and changes in immune function. Research hotspots gradually shifted from early topics such as differentiation, activation, memory, and mTOR related immunometabolic mechanisms to the tumor microenvironment, immunosuppression, single cell analysis, efficacy evaluation, and model construction. Literature derived high frequency gene terms highlighted immune regulatory clues, including CD4, STAT3, and CD44, as well as metabolic flow related clues, including HK2, PFKFB3, LDHA, and PC. The PubMed clinical subset further showed that mitochondrial function, glycolytic changes, trained immunity, and cell therapy related metabolic states have been investigated in disease state identification, therapeutic response monitoring, and cell therapy optimization. This study quantitatively and visually evaluated the overall development of immune cell metabolic reprogramming research. The findings suggest that the field is moving from single pathway descriptions toward a research model that integrates immune cell stratification, disease context stratification, and context specific translational investigation. By integrating the research landscape, thematic structure, molecular clues, and clinical entry points, this study provides candidate directions for independent molecular, functional, and clinical validation in immunometabolism.
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5. ABO genotyping proficiency testing: methodological strengths and outstanding issues requiring consideration.
PMID:日期:2026-09-22Development of proficiency testing (PT) for ABO genotyping is of great importance for the purpose of standardization and quality control in transplantation and histocompatibility laboratories. Hod-Dvorai et al. offer an interesting experience, describing a graded PT scheme that was developed and realized within a few years. The use of independently characterized materials for selected surveys may allow distinguishing between analytical errors and methodological trends, while the increase of allele diversity would contribute to the relevance of PT. These changes might improve the precision of grading and, indeed, participants feedback, thus further developing the framework suggested by the authors of the article.
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6. ATG7 rs1375206 Genotype as a susceptibility biomarker for preeclampsia in the Chinese Han population.
PMID:日期:2026-09-21Preeclampsia (PE) is linked to placental dysplasia and autophagy disorder. Atg7 is vital for placental development, yet its rs1375206 polymorphism with PE risk in Chinese Han population remains unclear. This study enrolled 990 PE patients and 1004 controls to genotype Atg7 rs1375206. Results revealed that this genetic variant was associated with susceptibility to preeclampsia (PE). Under the dominant genetic model (GG versus CG + CC, OR = 0.76, 95% CI 0.63-0.91, P = 0.003), carriers of the GG genotype exhibited lower PE risk compared with individuals carrying at least one C allele. Allelic comparison further verified that the C allele increased disease susceptibility compared with the G allele (OR = 1.33, 95% CI 1.17-1.51, P < 0.001). The recessive model (CC versus CG + GG, OR = 1.64; 95% CI, 1.29-2.07; P < 0.001) additionally confirmed a higher disease risk among CC homozygotes. The codominant comparison (CC vs CG vs GG) showed no significant difference in PE risk between CG heterozygotes and GG homozygotes (P = 0.102), whereas CC homozygotes exhibited substantially elevated risk relative to both CG heterozygotes and GG homozygotes (CC vs CG: OR = 1.52, 95% CI 1.19-1.95, P < 0.001; CC vs GG: OR = 1.79, 95% CI 1.39-2.32, P < 0.001). Stratified analysis showed differences in PE severity and onset subgroups. Bioinformatics and IHC confirmed reduced Atg7 expression in PE placentas. Atg7 rs1375206 may be associated with PE risk and serve as a potential genetic marker.
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7. Immunoinformatics-driven design and in silico characterization of a multiepitope vaccine targeting the hepatitis C virus core protein.
PMID:日期:2026-09-20Hepatitis C virus (HCV) remains a major global health burden, and its core protein is central to both viral replication and immune evasion. Here, we used an immunoinformatics approach to design a multiepitope vaccine directed against the HCV core protein. Several prediction platforms were applied to identify immunogenic regions that were antigenic, non-toxic, and non-allergenic; the twenty epitopes that met all of these criteria were joined by linkers and fused to 50S ribosomal protein L7/L12 and Pam2Cys adjuvants. The resulting construct was modeled, refined, and docked with Toll-like receptors (TLR2, TLR3, TLR4, TLR7, and TLR9), after which normal mode analysis (NMA) and molecular dynamics (MD) simulations were performed to assess its stability. The refined fusion protein showed favorable predicted binding to all of the receptors tested, and both NMA and MD indicated that the vaccine-TLR2 complex was conformationally stable. Immune simulation further predicted the production of anti-HCV antibodies and the activation of cellular immunity. Taken together, these findings identify the construct as a promising HCV vaccine candidate that now warrants experimental validation.
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8. Roles of the HLA-G gene and its polymorphisms in renal transplantation.
PMID:日期:2026-09-17Human leukocyte antigen-G (HLA-G) is a nonclassical major histocompatibility complex (MHC) class Ib molecule that plays a critical role in immune tolerance, primarily by promoting immune escape and inducing T-cell anergy. Early studies of HLA-G focused mainly on its function during pregnancy, where it is essential for maintaining maternal-fetal tolerance. In recent years, accumulating evidence has revealed the broader immunoregulatory functions and mechanisms of HLA-G in a variety of pathological conditions. As a key immunosuppressive molecule, HLA-G has been extensively investigated in the context of organ transplantation. In this review, we summarize the current understanding of the biological functions of HLA-G, with particular emphasis on its genetic polymorphisms, and discuss their immunomodulatory roles in renal allograft rejection and post-transplant infections.
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9. Self-amplifying RNA and circular RNA vaccines: mechanisms, delivery strategies, and prospects for long-lasting immunity.
PMID:日期:2026-09-17Messenger RNA vaccines have demonstrated extraordinary success during the COVID-19 pandemic, yet conventional mRNA platforms exhibit inherent limitations including modest molecular stability, stringent cold-chain requirements, waning antibody responses, and the necessity for relatively high doses to achieve protective immunity. Next-generation RNA technologies-specifically self-amplifying RNA (saRNA) and circular RNA (circRNA) vaccines-address these shortcomings through fundamentally distinct molecular designs that enhance antigen expression kinetics and prolong immunological persistence. Self-amplifying RNA vaccines incorporate viral replicase elements derived from alphaviruses, enabling intracellular amplification of the antigen-encoding sequence and sustained protein production at doses substantially lower than conventional mRNA. Circular RNA vaccines feature covalently closed loop structures that confer complete resistance to exonuclease-mediated degradation, extending translational half-life and maintaining antigen presentation over extended periods. This review provides a comprehensive examination of the molecular architecture, intracellular processing mechanisms, and immune activation pathways characteristic of both platforms. We critically evaluate formulation and delivery strategies, with particular emphasis on lipid nanoparticles and emerging carrier systems, and assess manufacturing challenges related to scalability, purity, and quality control. The preclinical and early clinical evidence supporting both platforms is synthesized and compared, highlighting the dose-sparing capacity of self-amplifying RNA and the exceptional durability of circular RNA-induced responses. Persistent obstacles-including reactogenicity modulation, circularization efficiency, replicase-associated innate suppression, and regulatory standardization-are analyzed in depth. We conclude by identifying priority research directions essential for clinical translation, including optimized delivery systems, refined safety profiling, and cold-chain-independent formulations that will enable global vaccine accessibility.
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10. Impact of the functional ERAP2 rs2248374 polymorphism on the HLA class I immunopeptidome in primary human epidermal keratinocytes.
PMID:日期:2026-09-14Endoplasmic reticulum aminopeptidase 2 (ERAP2) trims endogenous peptides before loading onto Human leukocyte antigen (HLA) class I molecules. A common polymorphism in ERAP2 (rs2248374) causes nonsense-mediated decay of ERAP2 mRNA, resulting in loss of protein expression. This polymorphism is associated with several HLA class I-associated inflammatory diseases including psoriasis. This study aimed to determine whether this specific polymorphism is sufficient to drive measurable differences in HLA-C expression and HLA class I immunopeptidome in primary human epidermal keratinocytes (HEKs). HEKs from 34 healthy donors were genotyped for ERAP2 (rs2248374) and HLA-C (rs4406273). HLA-C expression was assessed by flow cytometry. The immunopeptidome was isolated by immunoaffinity purification and analysed by liquid chromatography-mass spectrometry. HLA-C expression and global immunopeptidome features, including peptide yield, length distribution, and amino acid composition, were comparable across ERAP2 genotypes. However, ERAP2 genotype was associated with differences in peptide repertoire with the presence of genotype-specific peptides, an effect that became more pronounced in HLA-C*06:02-positive donors and even more among predicted HLA-C*06:02 majority-voted binder peptides. Within this HLA-C*06:02-stratified context, distinct sequence and chemical composition at the P1 anchor position also emerged. This suggests that the impact of ERAP2 is strongly context-dependent and partially masked in heterogeneous HLA settings.