CYTOKINE & GROWTH FACTOR REVIEWS细胞因子与生长因子评论
CYTOKINE & GROWTH FACTOR REVIEWS(英文缩写 CYTOKINE GROWTH F R),ISSN 1359-6101,eISSN 1879-0305,中文译名:细胞因子与生长因子评论 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：2025-11-01 至 2026-10-31，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 | 17.660 | Q1 |
| 2022 | 13.000 | Q1 |
| 2023 | 9.300 | Q1 |
| 2024 | 11.800 | Q1 |
| 2025 | 13.400 | Q1 |
CYTOKINE & GROWTH FACTOR REVIEWS 最新收录文献
-
1. Cytokine and chemokine dysregulation by Endocrine Disrupting Chemicals (EDCs).
1. 内分泌干扰化学物质（EDCs）导致的细胞因子和趋化因子失调PMID:日期:2026-09-26Endocrine-disrupting chemicals (EDCs) are traditionally defined by their ability to interfere with hormonal signalling. However, increasing evidence indicates that their biological effects also involve interactions with the immune system, particularly through the modulation of cytokine and chemokine networks. This review examines the relationship between EDC exposure and cytokine and chemokine dysregulation across major classes of endocrine disruptors, considering evidence from in vitro, in vivo, and epidemiological studies. Overall, EDCs can alter the production and regulation of inflammatory and immunoregulatory cytokines and chemokines, including mediators involved in both acute and chronic inflammatory responses. Depending on the chemical and exposure context, these alterations may result in either enhanced inflammatory signalling or suppression of immune responses. Importantly, cytokine dysregulation does not appear to represent an isolated effect of EDC exposure, but may be part of a broader interaction between endocrine and immune signalling. Changes in cytokine activity can, in turn, affect endocrine pathways and tissue homeostasis, suggesting a potentially bidirectional relationship between hormonal and immune regulation. These responses are highly dependent on the specific chemical, dose, exposure duration, tissue, developmental stage, and biological context. Although cytokine/chemokine alterations are consistently reported, direct evidence that these alterations mediate endocrine or systemic outcomes remains limited. A better understanding of this endocrine-immune interaction may provide a broader framework for interpreting the systemic effects of EDC exposure and for assessing endocrine disruption beyond conventional hormonal endpoints.
-
2. The multiple roles of TMEDs in viral infection and immune response.
2. TMED在病毒感染和免疫反应中的多重作用PMID:日期:2026-09-17The TMED proteins (transmembrane emp24 domain-containing) serve as essential regulators of the early secretory pathway and intracellular protein transport. This review focuses on their emerging roles in viral infection and innate immune control. We discuss how TMED10 mediates unconventional secretion of pro‑inflammatory factors and the SARS‑CoV‑2 spike protein, and highlight its involvement in vaccinia virus entry and in an immune evasion mechanism used by murine cytomegalovirus. Recent evidence also points to TMED9 as a modulator of RNA virus replication. At the level of innate immunity, TMED2 potentiates the MITA/STING pathway, while TMED2 and TMED7 contribute to Toll‑like receptor trafficking. Together, these observations point to the TMED family as a potential hub for therapeutic intervention against viral infections and inflammatory pathologies.
-
3. Inflammasome-autophagy crosstalk in the tumor microenvironment.
PMID:日期:2026-09-13The NLRP3 inflammasome has emerged as a critical sensor of cellular stress within the tumor microenvironment (TME), where its context-dependent activation can exert paradoxical effects on tumor progression and antitumor immunity. Diverse tumor-associated stressors, including mitochondrial dysfunction, reactive oxygen species (ROS), mitochondrial DNA (mtDNA) release, and cGAS-STING signaling, converge on NLRP3 activation, promoting caspase-1-dependent cytokine maturation and gasdermin D (GSDMD)-mediated pyroptosis. However, persistent or dysregulated inflammasome signaling may instead establish an immunosuppressive TME by modulating myeloid-derived suppressor cells (MDSCs), tumor-associated macrophages (TAMs), and immune checkpoint responses, thereby facilitating tumor immune escape and progression. A key emerging dimension of this regulatory network is the bidirectional crosstalk between NLRP3 signaling and autophagy, particularly mitochondria-selective mitophagy. Autophagic clearance of damaged mitochondria can restrain inflammasome activation by limiting mitochondrial danger signals, whereas inflammasome-driven inflammatory and metabolic remodeling can reciprocally reshape autophagic responses. This review integrates these traditionally studied pathways into a unified NLRP3-autophagy-mitochondrial stress axis and examines how its stage-, cell-, and context-dependent regulation determines tumor fate. We further critically evaluate pharmacological modulators targeting NLRP3 and autophagy, highlighting opportunities for dual-targeting strategies to simultaneously modulate tumor-intrinsic stress responses and tumor-extrinsic immunity. Overall, defining this mechanistic interface may uncover actionable vulnerabilities and provide a framework for developing context-specific combination therapies that enhance anticancer efficacy.
-
4. Mechanism and clinical relevance of metabolic-immune cross-talk in pancreatic tumor microenvironment.
PMID:日期:2026-09-12Metabolic stress-induced immunosuppression begins as early as the precancerous stage in pancreatic ductal adenocarcinoma (PDAC), increases with disease progression, and is characterized by the abundant suppressive myeloid and lymphoid cells. Metabolic adaptation and reprogramming are critical for the survival and function of tumor-infiltrating immune cells. In particular, cytotoxic T cells and natural killer (NK) cells, the stalwarts of cell-mediated immunity, often fail to adapt to the metabolically distinct pancreatic tumor microenvironment (TME) and thus perform antitumor activities poorly, leading to immune exhaustion, aggressive disease progression, metastasis, and poor immunotherapy outcomes. This review article explores the intricate metabolic-immune crosstalk, mediated by tumor microenvironment-associated factors, that impacts the metabolic fitness and effector functions of infiltrating immune cells, including cytotoxic T cells, NK cells, and myeloid cells that bridge innate and adaptive immunity. In addition, we discuss how genetic, molecular, and stromal factors drive metabolic alterations in nutrient-deficient pancreatic tumors, leading to immune cell dysfunction, impaired cytokine release, and poor antitumor immunity. This review further emphasizes the selective targeting of metabolic stress-driven immunosuppressive pathways, unresolved questions, and future directions, including how spatial nutrient gradients across the TME shape distinct regional immune phenotypes, how metabolic interactions with tumor and immune cells occur, and how tumor-selective metabolic therapies could be engineered to exploit features such as hypoxia and acidosis. Understanding these metabolic interactions is crucial for advancing personalized immunotherapy approaches, including immune checkpoint blockade therapies, CAR-T, and other adoptive immune cell therapies, which could improve clinical outcomes in PDAC patients.
-
5. Mechanistic analysis of immune communication during respiratory viral infections via the placenta-brain axis.
PMID:日期:2026-08-31Respiratory viral infections during pregnancy can disrupt maternal immune homeostasis, thereby altering placental function and fetal neurodevelopment through cytokine-mediated immune communication. Accumulating evidence suggests that the placenta functions as an active immunological interface, integrating maternal inflammatory signals and shaping fetal neuroimmune development, supporting the concept of the "placenta-brain axis". This review synthesizes current evidence on the cytokine, chemokine, interferon, and complement networks that mediate maternal-fetal immune communication and examines how these pathways are engaged during infections. It addresses four prevalent RNA respiratory viruses for which evidence is available at one or more biological levels of the placenta-brain axis, namely influenza virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), human respiratory syncytial virus (hRSV), and human metapneumovirus (hMPV). We highlight substantial differences in the depth of mechanistic evidence across these pathogens, with influenza virus and SARS-CoV-2 supported by comparatively robust experimental evidence, whereas hRSV and hMPV remain biologically plausible but mechanistically underexplored models of maternal-fetal immune communication. Hence, we propose a framework that grades mechanistic evidence across the placenta-brain axis against four explicit criteria and identify gestational timing, fetal sex, and maternal background inflammation as variables that modulate the transmission of inflammatory signals between levels. This structured approach identifies knowledge gaps and guides future mechanistic and translational research.
-
6. AMPK and macrophage crosstalk in diabetes: Mechanisms, inflammation, and therapeutic perspectives.
6. 糖尿病中AMPK与巨噬细胞的交互作用：机制、炎症及治疗前景PMID:日期:2026-08-20Diabetes mellitus, especially type 2 diabetes (T2DM), is a complex metabolic disease marked by persistent low-grade inflammation and insulin resistance. In diabetes, adipose tissue macrophages adopt a pro-inflammatory M1 phenotype, secreting cytokines including TNF-α, IL-6, and IL-1β that disrupt insulin signaling and cause metabolic dysfunction. AMP-activated protein kinase (AMPK), a cellular energy sensor, is a key regulator of macrophage polarization. It suppresses M1 responses by inhibiting NF-κB and JNK signaling, activating CREB/SIRT1 pathways, and promoting oxidative metabolism. Therefore, this review investigates the bidirectional interaction between AMPK signaling and macrophage function in diabetes, focusing on how metabolic stress affects AMPK activity, increasing inflammation and insulin resistance, whereas AMPK activation restores immune-metabolic balance. The gut microbiome further influences this axis, with short-chain fatty acids activating AMPK via GPR41/43, promoting M2 polarization and improving metabolic outcomes. Metformin, SGLT2 inhibitors, new direct AMPK activators such as PXL770, and lifestyle changes are also potential therapeutic treatments. However, considerable hurdles remain, including the prevalence of preclinical findings, a lack of macrophage-specific AMPK activators, simplicity of the M1/M2 paradigm, and uncertainty about long-term safety. Future research must focus on macrophage-targeted drug delivery, tissue-specific regulatory networks, biomarker discovery, and rigorous clinical trials with immunological outcomes. In conclusion, the AMPK-macrophage axis is a critical immune-metabolic gatekeeper in diabetes, and targeting this pathway offers a potential technique for restoring immune-metabolic balance, while significant difficulties must be overcome before practical use.
-
7. Deciphering the pulmonary fibrosis niche: A single-cell transcriptomic perspective on cellular crosstalk and microenvironment remodeling.
PMID:日期:2026-08-20Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal interstitial lung disease driven by aberrant repair after repetitive alveolar micro-injury. The classical paradigm - that fibrosis is a passive consequence of epithelial injury followed by fibroblast activation - has been substantially reshaped by single-cell RNA sequencing (scRNA-seq) and, more recently, spatial transcriptomics. These technologies have resolved the lung into a constellation of molecularly distinct cell states and exposed a highly structured fibrotic niche in which epithelial, mesenchymal, immune, and endothelial compartments are engaged in active, ligand-receptor-mediated crosstalk. This review synthesizes the emerging single-cell and spatial atlas of human PF/ILD, with a focus on four themes: (i) the ectopic KRT5⁻/KRT17⁺ aberrant basaloid epithelium and the persistence of a KRT8⁺ alveolar differentiation intermediate; (ii) the lipofibroblast-to-myofibroblast trajectory and the collagen-producing fibroblast atlas that explains heterogeneous drug response; (iii) immune remodeling, particularly the metabolic reprogramming of SPP1⁺/MERTK⁺ macrophages and the exhaustion of CD8⁺ T cells; and (iv) the spatial organization of disease-associated niches at the fibroblast-focus edge. We then translate these findings into a framework for molecular subtyping and precision medicine, arguing that the future of IPF therapy lies in disrupting specific niche communication axes rather than broadly antagonizing collagen synthesis. Beyond cataloguing cell types, we emphasize the systems-level principle that emerges from the single-cell literature: IPF is not a disease of one cell type gone wrong, but a disease of the communication network that binds multiple compartments into a self-sustaining, maladaptive ecosystem.
-
8. TRAF3IP2 (Act1/CIKS) variants: A domain to phenotype framework and therapeutic implications.
8. TRAF3IP2（Act1/CIKS）变异体：从结构域到表型的框架及治疗意义PMID:日期:2026-08-18Interleukin-17 (IL-17) family cytokines drive protective mucocutaneous immunity and, when dysregulated, a broad spectrum of inflammatory and autoimmune disease; almost all IL-17 receptor signaling converges on a single cytoplasmic adaptor, TRAF3IP2 (Act1/CIKS). This 574-amino-acid protein and U-box E3 ubiquitin ligase couples the IL-17 receptor to NF-κB and mitogen-activated protein kinase activation and also integrates non-IL-17 inputs through TRAF6, TRAF2/TRAF5, and TRAF3. Human germline variation in TRAF3IP2 offers a natural dissection of this adaptor along its signaling modules. Common coding variants that weaken TRAF6 recruitment, mainly rs33980500 (p.Asp19Asn), increase susceptibility to psoriasis and psoriatic arthritis, whereas rare biallelic variants that abolish SEFIR-mediated IL-17 receptor coupling cause chronic mucocutaneous candidiasis; an intermediate SEFIR lesion produces discoid lupus erythematosus. Additional associations span systemic lupus erythematosus, inflammatory bowel disease, cardiovascular disease, and malignancy. Interpreting these alleles has been limited by the absence of a variant catalogue anchored to a single protein reference and by a +9-residue offset between the 574- and 565-amino-acid isoforms that has propagated numbering errors across the literature. Here we assemble a reference-aligned atlas of 17 functionally or clinically annotated TRAF3IP2 variants on the 574-amino-acid sequence (NP_671733.2) and map each to the signaling interaction it perturbs. The resulting domain-to-phenotype framework, advanced as hypothesis-generating rather than deterministic, organizes variant effects along the IL-17 signaling axis, distinguishing TRAF-recruitment perturbation from receptor-coupling failure, and identifies the adaptor surfaces whose selective pharmacologic disruption could attenuate IL-17-driven inflammation in cardiovascular and oncologic disease while sparing antifungal immunity.
-
9. Molecular mechanisms of biologic and targeted synthetic antirheumatic drugs in rheumatoid arthritis.
PMID:日期:2026-08-12Rheumatoid arthritis is sustained by a synovial cytokine network that acquires the capacity to maintain inflammation independently of its initiating stimulus. The biologic and targeted synthetic antirheumatic drugs developed over the past two decades each interrupt this network at a defined molecular node, and their differential effects in patients therefore reveal how the network is organized. This review is structured around that principle, treating each agent as a probe of the axis it targets rather than as a therapeutic option. Following an account of the synovial signaling nodes on which diverse cytokines converge, four axes are examined: TNF-NF-κB, where receptor-level bifurcation between inflammatory and regulatory signaling defines the class; IL-6 and JAK-STAT, where classic and trans-signaling separate pathogenic from homeostatic function; costimulatory and lymphocyte-directed signaling, targeted by CTLA4-Ig and B-cell depletion; and the effector axes of tissue destruction driven by RANKL and GM-CSF. A recurring theme is that persistent synovitis reflects failure of the circuits that normally terminate cytokine signaling, and that fibroblast programs, once epigenetically imprinted, become progressively independent of the cytokines that established them. Synovial pathotypes correspond to differences in which axis is transcriptionally dominant, providing a biological rationale for stratified therapy; the same framework identifies a fibroblast-dominant state refractory to every current agent. Whether axis dominance is fixed or shifts under treatment remains the central unresolved question determining whether mechanism-guided therapy is clinically achievable.
-
10. Cytokine circuitries as determinants of response, resistance, and toxicity across cancer immunotherapy platforms.
10. 细胞因子网络作为跨癌症免疫治疗平台反应、耐药性和毒性的决定因素PMID:日期:2026-08-12[中文摘要] 癌症免疫治疗已显著改善了实体瘤和血液系统恶性肿瘤的治疗格局；然而，持久的临床获益仍受限于原发性和获得性治疗耐药、免疫相关毒性以及患者间显著的异质性。尽管细胞因子、趋化因子和生长因子作为预测性和预后性生物标志物已被广泛研究，但其在动态免疫网络中的协同功能仍未充分整合到当前的转化和临床框架中。本综述旨在批判性评估支持细胞因子网络动态的新兴证据，并引入适应性细胞因子回路（adaptive cytokine circuitries）这一概念框架，以理解相互连接的细胞因子信号如何在免疫检查点阻断、嵌合抗原受体T细胞治疗、T细胞受体工程化疗法、双特异性抗体及新兴细胞免疫治疗中调控治疗反应、耐药和毒性。现有证据表明，细胞因子相互作用通过空间和时间上组织化的信号网络发挥作用，影响T细胞功能状态、髓系细胞重编程、免疫逃逸和组织特异性炎症反应，同时凸显了重要的生物学不确定性以及前瞻性临床验证的必要性。本综述进一步探讨了纵向免疫监测、多重细胞因子谱分析、空间和单细胞多组学技术、计算网络重建以及生物标志物指导的患者分层在精准免疫治疗中的转化潜力。总体而言，现有证据支持从静态细胞因子测量向动态细胞因子网络分析的转变，同时强调了在细胞因子回路指导的策略能够在精准免疫肿瘤学中实施之前必须解决的科学和临床挑战。
[英文摘要] Cancer immunotherapy has substantially improved the management of solid tumors and hematologic malignancies; however, durable clinical benefit remains limited by primary and acquired therapeutic resistance, immune-related toxicities, and considerable interpatient heterogeneity. Although cytokines, chemokines, and growth factors have been extensively investigated as predictive and prognostic biomarkers, their coordinated functions within dynamic immune networks remain insufficiently integrated into current translational and clinical frameworks. The purpose of this review is to critically evaluate emerging evidence supporting cytokine network dynamics and to introduce adaptive cytokine circuitries as a conceptual framework for understanding how interconnected cytokine signaling regulates therapeutic response, resistance, and toxicity across immune checkpoint blockade, chimeric antigen receptor T-cell therapy, T-cell receptor-engineered therapies, bispecific antibodies, and emerging cellular immunotherapies. Current evidence indicates that cytokine interactions operate through spatially and temporally organized signaling networks that influence T-cell functional states, myeloid cell reprogramming, immune escape, and tissue-specific inflammatory responses, while highlighting important biological uncertainties and the need for prospective clinical validation. The review further examines the translational potential of longitudinal immune monitoring, multiplex cytokine profiling, spatial and single-cell multi-omic technologies, computational network reconstruction, and biomarker-guided patient stratification for precision immunotherapy. Collectively, the available evidence supports a transition from static cytokine measurements toward dynamic cytokine network analysis while underscoring the scientific and clinical challenges that must be addressed before cytokine circuitry-informed strategies can be implemented in precision immuno-oncology.