IMMUNOLOGY AND CELL BIOLOGY免疫学与细胞生物学
IMMUNOLOGY AND CELL BIOLOGY(英文缩写 IMMUNOL CELL BIOL),ISSN 0818-9641,eISSN 1440-1711,中文译名:免疫学与细胞生物学 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 | 5.853 | Q2 |
| 2022 | 4.000 | Q3 |
| 2023 | 3.200 | Q3 |
| 2024 | 3.000 | Q3 |
| 2025 | 3.300 | Q3 |
IMMUNOLOGY AND CELL BIOLOGY 最新收录文献
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1. Unmasking the Influence of Viral Micro-RNAs on Host Immunity.
PMID:日期:2026-09-22Micro-RNAs (miRNAs) are key regulators of human immunity, controlling critical cellular programmes including proliferation, differentiation, apoptosis, and immune activation to shape the host response to infection. Multiple human-infecting viruses encode their own miRNA (v-miRNA), enabling them to co-opt host gene regulatory machinery to subvert immunity, establish persistence and evade immune-mediated killing. This review synthesizes the current evidence on viral miRNAs and their roles in host-virus interactions, with an explicit focus on immune regulation. We examine how different viruses use v-miRNAs to modulate core immune functions, including antigen presentation, cytokine signaling, NK and CD8 T-cell activation, and apoptosis. We also examine how v-miRNAs manipulate viral gene expression to aid immune evasion and promote persistence. Particular emphasis is placed on experimentally validated immune targets and their clinical consequences. Collectively, these examples illustrate the convergent evolution of v-miRNA-mediated immune evasion across diverse viral families. Understanding this class of molecules will provide insight into critical immune evasion strategies employed by clinically important viruses and may identify novel targets for diagnostic and antiviral therapeutics, including antagomir-based and RNA silencing approaches.
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2. Hypercapnia Induces Mitochondrial Adaptations and Alters Glutamine Metabolism to Drive a Distinct Metabolic Phenotype in Monocytes.
2. 高碳酸血症诱导线粒体适应并改变谷氨酰胺代谢以驱动单核细胞形成独特的代谢表型PMID:日期:2026-09-16Carbon dioxide (CO) is an ancient and ubiquitous physiological gas generated during aerobic respiration. Historically viewed as a simple metabolic waste product, CO has received far less research attention than oxygen (O), the primary substrate of aerobic respiration. However, emerging evidence has revealed important roles for CO in immunometabolism, immunology, muscle physiology, and clinical medicine. While circulating pCO levels are tightly regulated, patients with lung diseases such as chronic obstructive pulmonary disease (COPD) frequently develop hypercapnia, pCO > 45 mmHg. Hypercapnia is associated with significantly increased mortality, higher risk of ICU admission, and a global prevalence estimated at 13-15 million patients. Its broader clinical consequences remain poorly understood and are inadequately integrated into current therapeutic paradigms. Here, we examined the impact of hypercapnia on the metabolic profile of monocytes. We demonstrate that 24 h of buffered hypercapnia induces a marked reduction in mitochondrial mass. This is accompanied by dysregulation of mitochondrial membrane potential and key bioenergetic substrates (NADH/NAD and ATP content). We further show that hypercapnia alters the abundance of metabolites and proteins associated with mitochondrial metabolism, with effects spanning glucose, glutamine, and lipid metabolism. Thus, we provide direct mechanistic evidence that hypercapnia directly alters the glutamine-glutamate-proline synthesis axis. Collectively, these findings establish the foundation for a discrete hypercapnic metabolic phenotype, that is, in several respects, distinct from the metabolic adaptations observed in hypoxia. We propose that hypercapnia triggers a cascade of metabolic adaptations with tissue-dependent consequences on cellular effector functions.
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3. Role of T Cells in Chronic Pain: Mechanisms, Regulation, and Therapeutic Implications.
PMID:日期:2026-09-06T cells are critical for controlling the adaptive immune response and maintaining the homeostasis of the body. Recent evidence suggests that T cells are involved in the initiation, maintenance, and resolution of chronic pain by releasing mediators such as cytokines and endogenous opioids. In this review, we highlight recent advances in the involvement of T cells in chronic pain. We also describe how T cells act on sensory neurons to promote, suppress, or even resolve pain. Finally, we review how T cells are regulated and how we can translate these findings to develop therapies for chronic pain.
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4. Carbocisteine Reduces Airway Mucus Obstruction and Alters Inflammatory Cell Populations in a Model of Muco-Obstructive Lung Disease.
PMID:日期:2026-09-01Muco-obstructive lung diseases, including chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), and bronchiectasis, are characterized by excessive mucus production, airway surface dehydration, impaired mucociliary clearance, and progressive lung function decline. As the efficacy of current therapies often declines with muco-obstructive disease progression, contributing significantly to morbidity and mortality, there is a need for improved treatments that address underlying defects in mucus homeostasis and airway physiology. In this study, we evaluate the effects of carbocisteine, a mucoactive therapeutic, in the βENaC-transgenic (βENaC-Tg) model of muco-obstructive lung disease. Short-term carbocisteine administration significantly reduced airway mucus obstruction, potentially through decreased concentrations of Muc5ac and Muc5b. Notably, carbocisteine treatment modulated key inducers of mucus production, such as interleukin (IL)-13 and the upstream promoter cytokine IL-17, suggesting broader effects on mucoregulatory pathways. Carbocisteine administration was observed to alter mononuclear cell populations, impacting specific inflammatory subsets of CD11b alveolar macrophages and Ly6c monocytes, indicating immunomodulatory effects, either directly or secondary to improved mucus clearance. However, despite changes in immune cell populations, short-term administration failed to mitigate lung damage and inflammation associated with established muco-obstructive lung disease. These findings demonstrate the potent mucoactive effect of carbocisteine in established muco-obstructive lung disease, through a broader mechanism of action than previously understood, with the potential to modulate inflammatory responses for preventive or long-term treatment strategies.
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6. The N6-Methyladenosine-Modified CIT Promotes Uterine Corpus Endometrial Carcinoma Progression by Inhibiting the Hippo Signaling Pathway.
PMID:日期:2026-09-01This study investigates the role of CIT gene in uterine corpus endometrial carcinoma (UCEC) progression, focusing on its regulation by m6A methylation. Bioinformatics and experimental analyses (EdU, colony formation assay, Dot blot, MeRIP-PCR, RNA pull-down, qRT-PCR, Western Blotting, apoptosis assay) revealed that CIT was significantly overexpressed in UCEC. Mechanistically, we found that the m6A writer RBM15-mediated CIT mRNA methylation, which was then recognized by the reader IGF2BP1 to enhance CIT mRNA stability and expression. Consequently, this m6A-mediated upregulation of CIT inhibited the Hippo signaling pathway, ultimately suppressing apoptosis and promoting malignant proliferation in UCEC. These findings elucidated a novel RBM15/IGF2BP1-CIT-Hippo axis, providing new theoretical insights and potential therapeutic targets for UCEC.
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7. Molecular insights into the anti-inflammatory and antifibrotic effects of licorice-ginger decoction in experimental models of inflammatory arthritis-associated lung fibrosis.
7. 甘草姜汤在炎症性关节炎相关肺纤维化实验模型中抗炎和抗纤维化作用的分子见解PMID:日期:2026-09-01Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a severe autoimmune complication lacking effective treatments. This study investigates the molecular mechanisms underlying the therapeutic effects of licorice-ginger decoction (GGD) in experimental models relevant to arthritis-associated lung fibrosis. Utilizing network pharmacology, transcriptomic sequencing, and molecular docking analyses, we identified the STAT1/ICAM1/IL-17A signaling pathway as crucial for GGD efficacy. Experimental validation in both cellular and murine models demonstrated that GGD markedly alleviated body weight loss, reduced arthritis severity, and improved pulmonary pathological injury under inflammatory arthritis conditions. Mechanistic analyses revealed direct binding of Kae and QR to STAT1/ICAM1, leading to IL-17A inhibition and mitigation of epithelial-mesenchymal transition (EMT) and fibroblast activation. Notably, overexpression of STAT1 attenuated the therapeutic effects of GGD. This study provides mechanistic insights into the anti-inflammatory and antifibrotic effects of GGD in experimental models relevant to arthritis-associated lung fibrosis and offers a potential framework for future mechanistic studies and translational research of classical Chinese formulations.
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8. The Emerging Role of UCHL1 in Neurological and Musculoskeletal Diseases.
8. UCHL1在神经和肌肉骨骼疾病中的新作用PMID:日期:2026-09-01Ubiquitin C-terminal hydrolase L1 (UCHL1) is a highly conserved deubiquitinating enzyme that has transitioned from being viewed as a "brain-specific" protein to a global regulator of cellular proteostasis and signal transduction. As a key component of the ubiquitin-proteasome system (UPS), UCHL1 maintains the intracellular free ubiquitin pool through its C-terminal hydrolase activity, while also exhibiting atypical ligase-like functions and acting as a molecular scaffold for signaling complexes. Beyond its classical role in neurons, increasing evidence suggests that UCHL1 participates in diverse pathological conditions including neurodegeneration, cancer, cardiovascular and metabolic diseases, as well as musculoskeletal disorders. Through regulation of protein turnover, oxidative stress, inflammatory signaling, and cell survival, UCHL1 emerges as a context-dependent regulator with dual protective and pathogenic roles. This review explores the sophisticated multi-level regulation of UCHL1, ranging from transcriptional control to epigenetic silencing and posttranslational modifications, summarizes the recent research progress of UCHL1 in various systems, and elaborates on its mechanism of action in various conditions, including neurological and musculoskeletal disorders.
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9. Beyond the Human Body: Models for Studying Neutrophil Biology.
PMID:日期:2026-09-01Neutrophils are a key component of the immune system, integrating antimicrobial and immunomodulatory functions through various strategies, including phagocytosis, degranulation, generation of reactive oxygen species (ROS), and release of neutrophil extracellular traps (NETs). Owing to their complexity and involvement in a wide range of conditions, including autoimmune diseases, neutrophils have emerged as a major focus of biomedical research. However, it should be noted that neutrophil studies face significant challenges, including short lifespan, terminal differentiation, tendency to spontaneous activation, and donor variability. Moreover, resistance to genetic modifications limits the detailed investigation of gene function and signaling pathways in neutrophil biology. To overcome these constraints, a range of experimental models has been developed. In this review, we present a guide to the currently available neutrophil models (HSPC, iPSC, HL-60, PLB-985, NB4, Kasumi-1, ER-Hoxb8), highlighting their strengths and limitations, with particular emphasis on their value as genetically modifiable platforms. Additionally, we provide an insight into the mechanisms governing neutrophil effector functions.