IMMUNOLOGIC RESEARCH免疫学研究
IMMUNOLOGIC RESEARCH(英文缩写 IMMUNOL RES),ISSN 0257-277X,eISSN 1559-0755,中文译名:免疫学研究 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 | 4.505 | Q3 |
| 2022 | 4.400 | Q2 |
| 2023 | 3.300 | Q3 |
| 2024 | 3.100 | Q2 |
| 2025 | 2.700 | Q3 |
IMMUNOLOGIC RESEARCH 最新收录文献
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1. Augmenting antitumor immunity in colon cancer via GSDMD-mediated pyroptosis induced by an attenuated Salmonella delivery system.
PMID:日期:2026-10-05As a major gastrointestinal malignancy, colon cancer (CC) demands more effective therapies. Gene therapy is an emerging promising strategy, and pyroptosis, a novel lytic cell death form, serves as a vital antitumor target, with Gasdermin D (GSDMD)-a key pore-forming protein in pyroptosis-showing anti-CC potential. We constructed an engineered attenuated Salmonella strain to deliver a GSDMD-expressing plasmid, and verified its therapeutic efficacy via in vitro and in vivo studies. In CC cell lines, the Salmonella vector upregulated GSDMD and cleaved caspase-1 (its upstream activator), inhibiting cell proliferation and inducing pyroptosis. In CC-bearing mice, the strain significantly suppressed tumor progression, reduced Ki67 expression, elevated intratumoral GSDMD and cleaved caspase-1 levels, and enhanced CD4 and CD8 T cell infiltration to boost antitumor immunity. This study suggests that attenuated Salmonella-mediated GSDMD delivery combats CC by triggering pyroptosis and stimulating antitumor immunity, laying a foundation for GSDMD-targeted gene therapeutics.
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2. Vitamin D status and supplementation as potential modifiers of allergen immunotherapy outcomes in respiratory allergy: A structured narrative review.
PMID:日期:2026-10-02Allergen immunotherapy (AIT) represents a cornerstone in managing IgE-mediated allergic diseases, such as allergic rhinitis and asthma. By administering controlled doses of allergens over time, AIT aims to readjust immune tolerance, thereby modifying allergic responses. However, clinical responses to AIT remain heterogeneous, with a subset of patients achieving only partial benefit. This heterogeneity underlines the need for novel adjunctive approaches to potentiate the immunomodulatory effects of AIT. In this context, vitamin D has gained considerable interest, given its well-established role in immune homeostasis and regulation, as well as its emerging relevance in modulating allergic disease. This structured narrative review aims to assess the potential role of vitamin D supplementation during AIT on clinical outcomes as well as the significance of endogenous vitamin D levels on AIT clinical efficacy. A total of 18 studies were reviewed, 13 evaluating the impact of vitamin D supplementation during AIT and 5 assessing the influence of endogenous vitamin D levels on AIT outcomes. Most supplementation studies reported clinical outcomes favoring the addition of vitamin D to AIT, but three found no additional benefit, and two reported a benefit only at an earlier time point, respectively in vitamin D-deficient patients. Of the five studies examining endogenous status, three reported that higher 25-hydroxyvitamin D (25(OH)D) levels were associated with better AIT outcomes. Other findings that were reported as secondary outcomes included favorable immunologic changes, such as IL-10 production, decreased allergen-specific IgE levels, and enhanced regulatory Treg-cell activity, without formal assessment of their contribution to clinical benefit. Nevertheless, findings remain inconsistent across studies due to heterogeneity in study design, supplementation regimens, and outcome measures. While the available evidence suggests that adequate vitamin D status or supplementation may be associated with better clinical responses to AIT, the current findings remain limited by heterogeneity in study design, supplementation regimens, outcome measures, and generally small sample sizes. Therefore, the evidence should be considered suggestive rather than conclusive. Although correction of vitamin D deficiency is appropriate on general clinical grounds, its specific use as an adjunct to improve AIT outcomes cannot yet be routinely recommended. Further adequately powered, standardized, placebo-controlled studies are needed to clarify its role and inform clinical recommendations.
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3. Identification of genetic variants associated with monogenic autoinflammatory diseases in patients with Still's disease using next-generation sequencing.
3. 使用下一代测序技术鉴定斯蒂尔病患者中与单基因自身炎症性疾病相关的遗传变异PMID:日期:2026-10-01In this study, we aimed to identify potential variants associated with monogenic autoinflammatory diseases (AIDs) in patients with Still's disease (SD), thereby enhancing our understanding of the complex genetic mechanisms driving SD. This study included adult patients with SD who had available genetic data. Demographic characteristics, clinical findings, and laboratory test results were recorded. Genomic variants related to AIDs were detected using next-generation sequencing with a targeted gene panel for all coding exons and exon-intron boundaries of relevant genes. Identified variants were interpreted using multiple in silico prediction models and genomic databases and classified following the 2015 ACMG/AMP recommendations. Thirty-nine patients were included, of whom 19 (49%) carried at least one genetic variant. A total of 22 distinct variants were identified across 15 genes, including NLRP1, NLRP3, NLRP12, MEFV, LPIN2, IFIH1, PSMB8, IL10RA, IL10RB, IL36RN, SLC29A3, PLCG2, NOD2, CARD14, and SH3BP2. All variants were monoallelic; most were missense, whereas two were frameshift variants in IFIH1 and NLRP1. Most variants were classified as variants of uncertain significance, while variants in MEFV and IFIH1 were classified as pathogenic and likely pathogenic, respectively. Different genetic variants can be observed in patients with SD, and these variants are possibly epiphenomena rather than being Still's disease-driven mutations. Their presence may contribute to variability in clinical findings and disease course, which requires further investigation to be fully understood.
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4. Combined in vitro microcurrent stimulation and celecoxib suppress NF-κB/NLRP3 signaling and cartilage catabolism in human chondrocytes.
4. 体外微电流刺激联合塞来昔布抑制人软骨细胞中NF-κB/NLRP3信号通路及软骨分解代谢PMID:日期:2026-09-25Osteoarthritis is characterized by persistent inflammatory signaling, oxidative stress, chondrocyte dysfunction, and extracellular-matrix degradation. This study investigated whether controlled in vitro microcurrent stimulation could enhance the anti-inflammatory and chondroprotective effects of celecoxib in interleukin-1β (IL-1β)-challenged human chondrocytes. Immortalized C28/I2 chondrocytes and primary human knee articular chondrocytes were treated with celecoxib, microcurrent stimulation, or their combination. A factorial concentration-current matrix, Bliss-independence analysis, and two-way analysis of variance were used to evaluate interaction effects on IL-6 secretion. Selected inflammatory, anabolic, catabolic, NF-κB, COX-2/PGE₂, NLRP3-associated, oxidative-stress, mitochondrial, and apoptosis-related endpoints were examined at the submaximal combination of 2.5 µM celecoxib and 25 µA microcurrent stimulation. PGE₂ add-back and nigericin challenge experiments were performed to investigate the involvement of PGE₂- and NLRP3-associated signaling. IL-1β induced a pronounced inflammatory and catabolic phenotype. Celecoxib and microcurrent stimulation individually reduced selected inflammatory mediators, NF-κB signaling, matrix-catabolic markers, oxidative stress, and pyroptosis-associated endpoints. The celecoxib × microcurrent interaction for IL-6 inhibition was significant (F[12,40] = 3.67, P = 0.0009). Bliss analysis identified synergy in eight of the twelve nonzero combinations, whereas four combinations were not distinguishable from Bliss additivity. The greatest Bliss excess occurred with 25 µA microcurrent stimulation plus 2.5 µM celecoxib (18.0% points; 95% bootstrap confidence interval, 12.7-23.7). At this condition, combined treatment produced greater IL-6 and PGE₂ inhibition and more favorable MMP13 and COL2A1 responses than either monotherapy. Because formal factorial synergy analysis was performed only for IL-6, improvements in the other endpoints were interpreted as enhanced combined responses rather than demonstrated synergy. Combined treatment was associated with reduced MYD88 expression, NF-κB pathway phosphorylation and nuclear p65 localization, together with suppression of COX-2/PGE₂-associated signaling, lower NLRP3/caspase-1/GSDMD-related responses and oxidative stress, and preservation of selected mitochondrial indices. Exogenous PGE₂ and nigericin partially reversed selected responses, supporting pathway involvement without establishing causal necessity or dependency. Selected treatment responses were reproduced in primary human knee articular chondrocytes. Controlled in vitro microcurrent stimulation combined with celecoxib produced concentration- and current-specific Bliss synergy for IL-6 inhibition and enhanced selected inflammatory and matrix-protective responses. These findings support further evaluation in physiologically relevant cartilage and in vivo osteoarthritis models but should not be interpreted as evidence of clinical efficacy or equivalence to clinical electroacupuncture.
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5. CSF neuroinflammatory biomarkers are associated with amyloid-β42/40, tau pathology, and cognitive impairment across the Alzheimer's disease spectrum.
5. 脑脊液神经炎症生物标志物与阿尔茨海默病谱系中的淀粉样蛋白-β42/40、tau蛋白病理及认知障碍相关PMID:日期:2026-09-25Neuroinflammation is increasingly implicated in Alzheimer's disease (AD), but how distinct CSF inflammatory biomarkers relate to AD pathology remains unclear. This study examined whether CSF biomarkers reflecting astrocytic activation (GFAP), microglial activation (TREM2), systemic inflammation (CRP), TNF-related signaling (TNFR2), and inflammatory proteolysis (ADAM17) were associated with CSF Aβ42/40, CSF p-tau181, and cognitive performance across the AD clinical spectrum. Data were obtained from 933 ADNI participants, including 312 cognitively normal (CN) individuals, 471 participants with mild cognitive impairment (MCI), and 150 participants with AD dementia. Analyses were corrected for multiple comparisons using the FDR method. The results showed that CSF neuroinflammatory biomarkers differed across diagnostic groups, with GFAP showing the strongest progressive increase from CN to MCI and AD dementia. Higher GFAP, TREM2, TNFR2, and ADAM17 levels were associated with lower CSF Aβ42/40, higher CSF p-tau181, and poorer cognitive performance, particularly in MCI, whereas CRP showed weaker and less consistent associations. In joint models including all inflammatory and core AD biomarkers, both higher GFAP and higher TNFR2 remained independently associated with worse cognitive function. Mediation analyses showed that lower CSF Aβ42/40 partly mediated the associations of higher GFAP and TREM2 with worse cognitive performance. Higher CSF p-tau181 mediated broader associations linking higher GFAP, TREM2, TNFR2, and ADAM17 levels to worse cognitive performance, with the strongest effects observed in MCI. Overall, higher CSF neuroinflammatory biomarkers may be linked to AD pathology and cognitive impairment; however, given the observational design, causality cannot be established, and longitudinal mechanistic studies are needed to validate these findings.
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6. Pyroptosis in chronic obstructive pulmonary disease: Beyond the canonical NLRP3/Caspase-1/GSDMD pathway.
6. 慢性阻塞性肺疾病中的细胞焦亡：超越经典NLRP3/Caspase-1/GSDMD通路PMID:日期:2026-09-23Chronic obstructive pulmonary disease (COPD), the third leading cause of death worldwide, is characterized by persistent airway inflammation that remains incompletely controlled in some patients despite current anti-inflammatory therapies. Pyroptosis, a pro-inflammatory, lytic form of programmed cell death mediated by the gasdermin family of proteins, has emerged as a key amplifier of inflammation in COPD. Although most evidence centers on the NLR family pyrin domain-containing 3 (NLRP3)/caspase-1/gasdermin D (GSDMD) axis, COPD-relevant studies increasingly implicate non-canonical caspase-4/5/11-GSDMD signaling and alternative gasdermins. The evidence is hierarchical: GSDMD has the strongest cleavage-dependent support; gasdermin E (GSDME)-associated signaling has been linked experimentally to epithelial injury, whereas gasdermin C (GSDMC) and gasdermin B (GSDMB) are supported mainly by expression and stimulus-response data. We propose a "dual pyroptosis strike" model in which infection-associated non-canonical signaling may amplify a smoke-conditioned canonical background during acute exacerbations of COPD (AECOPD), while emphasizing that clinical execution-level validation remains lacking. This review synthesizes current findings into a conceptual gasdermin atlas, critically appraises cell-type- and disease-stage-specific findings, and discusses both therapeutic strategies and biomarker-guided approaches. Cleavage-resolved, cell-type-resolved, and longitudinal validation will be required before these pathways can inform patient stratification or targeted intervention.
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7. Drugging trained immunity: immunometabolic and epigenetic control of maladaptive inflammatory memory in chronic inflammatory diseases.
7. 药物调控训练免疫：慢性炎症性疾病中适应不良性炎症记忆的免疫代谢与表观遗传控制PMID:日期:2026-09-15Chronic inflammatory diseases are usually treated as persistent activation states, yet many disorders also contain a memory component: innate immune cells and their bone marrow progenitors can retain durable metabolic and epigenetic programs after infection, sterile injury, modified lipoproteins, crystals, diet or vaccination. This process, known as trained immunity, improves host defense when appropriately induced but may also amplify maladaptive inflammation in atherosclerosis, gout, rheumatoid arthritis, inflammatory bowel disease, neuroinflammation, chronic pain and metabolic disease. The pharmacological importance of trained immunity is increasing because its core mechanisms are druggable: glycolysis, mTOR-HIF-1 alpha signaling, the mevalonate pathway, tricarboxylic-acid-cycle metabolites, histone methylation and acetylation, chromatin accessibility, NLRP3 inflammasome activity and IL-1 beta signaling. This review critically synthesizes trained immunity as a disease-relevant inflammatory memory program and evaluates repurposed and emerging interventions, including colchicine, IL-1 blockers, statins, metformin, mTOR inhibitors, fumarate/itaconate-related metabolic modulators, BET/HDAC-directed epigenetic strategies and NLRP3 inhibitors. We propose a translational framework in which patients are stratified by inflammatory-memory phenotypes, interventions are matched to dominant metabolic-epigenetic modules, and treatment success is judged by durable resolution without excessive immunosuppression. This approach can help convert trained immunity from a descriptive immunological concept into a practical target class for inflammation pharmacology.
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8. The cost-benefit of newborn screening for X-linked agammaglobulinemia and related B-cell lymphopenia.
8. X连锁无丙种球蛋白血症及相关B细胞淋巴细胞减少症新生儿筛查的成本效益PMID:日期:2026-09-15Early detection of X-linked agammaglobulinemia (XLA) and other profound B cell lymphopenias (BCL) in newborns is crucial for timely intervention and improved clinical outcomes. The kappa light chain rearrangement excision circles (KREC) assay has emerged as an effective specific and sensitive tool for newborn screening (NBS) of XLA and other BCL. Large-scale studies have demonstrated that KREC-based NBS identifies affected infants before symptom onset, enabling prompt initiation of immunoglobulin replacement therapy (IGRT) and prophylactic antibiotics, thereby preventing recurrent infections, chronic organ damage, and reducing healthcare burden. Here, we evaluate the possible cost-benefit of NBS for XLA and other BCL. Economic evaluation shows that adding KREC screening to existing NBS programs is likely to be cost-effective and fulfills established criteria for NBS inclusion, supporting its adoption in universal NBS protocols.
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9. The spatial architecture of tumor immunity: Emerging predictive biomarkers across cancer.
9. 肿瘤免疫的空间结构：跨癌种的新兴预测性生物标志物PMID:日期:2026-09-12Tumor immunity is shaped not only by the cellular composition of the tumor microenvironment (TME), but also by its spatial architecture. Increasing evidence shows that immune function cannot be inferred from cell abundance alone, because the positioning and coordination of immune and stromal cells determine whether local immunity is activated, excluded, or suppressed. Advances in multiplex imaging, spatial proteomics, spatial transcriptomics, and AI-assisted tissue analysis now enable high-resolution mapping of these spatial states across clinically relevant scales. These approaches reveal that tumors are organized as recurrent microarchitectures that can function either as immune engines or as suppressive brakes. Immune-supportive structures, including mature tertiary lymphoid structures, dendritic cell-centered immune triads, high endothelial venule-associated recruitment corridors, and effector-tumor interfaces, promote antigen presentation, lymphocyte recruitment, and cytotoxic engagement. In contrast, exclusionary and suppressive architectures, such as CAF-mediated stromal barriers, SPP1 + macrophage-CAF niches, stalled T-cell zones, Treg-enriched suppressive niches, and NLRP3 + macrophage-rich regions, restrict infiltration and sustain immune dysfunction. Across cancer types, such spatial readouts are emerging as robust biomarkers. In this Review, we summarize recent progress in spatial tumor immunology and propose a conceptual framework for interpreting tumor immunity from composition to cellular neighborhoods. We further discuss how these spatial architectures shape tumor heterogeneity, therapeutic response, and resistance, and how they may be translated into actionable biomarkers for patient stratification, treatment monitoring, and next-generation precision immunotherapy.
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10. Clinical Course and Treatment Outcomes of Vulvar Condylomas in Immunocompromised Women: A Retrospective Cohort Study.
10. 免疫功能低下女性外阴尖锐湿疣的临床病程与治疗结局：一项回顾性队列研究PMID:日期:2026-09-12Human papillomavirus (HPV) infection is highly prevalent worldwide and is associated with a broad spectrum of anogenital diseases, including vulvar condylomas and malignancies. Immunosuppression plays a key role in HPV persistence, recurrence, and progression; however, data on the clinical course of vulvar condylomas in immunocompromised women remain limited. This retrospective cohort study evaluated clinical progression, treatment response, recurrence, and neoplastic outcomes in women diagnosed with vulvar condyloma between January 2008 and January 2021 at a tertiary referral center in Brazil. Immunosuppressed patients, including women living with HIV, those receiving immunosuppressive therapy for autoimmune diseases, and patients undergoing chemotherapy, were compared with an age-matched immunocompetent group. Among 294 women included, 41 (13.9%) were immunosuppressed. Lesion extent was significantly greater in immunosuppressed patients, although lesion number did not differ between groups. Clinical remission after first-line treatment was significantly lower among immunosuppressed women (21.9%vs55.0%; p < 0.0001; OR = 4.5) with a higher need for multiple treatment sessions. Similarly, the complete remission rate at the end of follow-up was higher for the immunocompetent patients (75.9% vs. 48.8%; p < 0.0001; OR = 3.3). Immunosuppressed women had a 2.3-fold increased risk of recurrence and a higher risk of progression to vulvar intraepithelial neoplasia (OR = 6.7) and invasive disease (OR = 8.5). In the HIV patients, recurrence was not associated with CD4T-lymphocyte count or HIV viral load. These findings indicate that immunosuppressed women with vulvar condylomas experience more extensive disease, poorer treatment response, higher recurrence rates, and an increased risk of neoplastic progression, highlighting the importance of closer surveillance and individualized management in this high-risk population.