Immunology最新文献

{"title":"Resilient Biophysical Phenotype of Memory CD4 ⁺ T Cells in Long-Lived Mice.","authors":"Aldo Abarca-Ortega, Blanca González-Bermúdez, Judith Félix-Escalera, Mónica González-Sánchez, Enzo Brito, Mónica De la Fuente, Gustavo R Plaza","doi":"10.1111/imm.70123","DOIUrl":"10.1111/imm.70123","url":null,"abstract":"<p><p>Age-related alterations in the immune system-collectively known as immunosenescence-include both quantitative and qualitative changes across various immune cell populations, including B cells, natural killer cells and T lymphocytes, affecting their structure, phenotype and function. While these changes have been characterised biochemically and physiologically, their biophysical manifestations remain less understood, particularly in individuals that achieve exceptional longevity. Here, we investigate the mechanical and structural properties of memory CD4⁺ T cells from mice across three aging stages: old (72 ± 4 weeks), very old (96 ± 4 weeks) and long-lived (> 120 weeks). We conducted a cross-sectional analysis combining micropipette aspiration, 3D confocal microscopy, spontaneous migration assays and flow cytometry to evaluate cellular stiffness, motility, nuclear morphology and cytoskeletal organisation. Our results confirm previous reports of increased stiffness and reduced migration in T cells from very old mice. However, this trend does not persist in long-lived individuals, who display mechanical and migratory properties similar to younger cohorts. Relative nuclear size (R _n/R _c) and actin organisation also stabilise in this group, suggesting the maintenance of intracellular architecture despite advanced chronological age. Notably, no significant changes were found in the expression levels or distribution of key structural proteins (actin, myosin, vimentin), nor in markers of DNA methylation (5-mC) or cellular senescence (p16). These findings support the concept of mechanical resilience in the immune system as a feature of successful aging, highlighting that certain biophysical traits may be preserved or selectively maintained in extreme longevity. This study provides novel evidence linking T cell mechanics with immune health and longevity and identifies candidate parameters for future investigations into aging biomarkers.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"363-374"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Determinants of Peanut-Specific IgG4 Levels in the Context of Sustained Oral Peanut Exposure in the LEAP Study.","authors":"Kanika Kanchan, Karen Cerosaletti, James A Perry, George DuToit, Monali Manohar, Hua Ling, Justin E Paschall, Srinath Sanda, R Sharon Chinthrajah, Gerald T Nepom, Kari C Nadeau, Stacie M Jones, Gideon Lack, Ingo Ruczinski, Rasika A Mathias","doi":"10.1111/imm.70098","DOIUrl":"10.1111/imm.70098","url":null,"abstract":"<p><p>In the Learning Early About Peanut Allergy (LEAP) study, participants in the peanut consumption group, at 60 months of age, had higher levels of peanut-specific IgG4 (psIgG4), a biomarker of immune modulation, compared to those in the peanut-avoidance group. We investigated the genetic determinants of psIgG4 among participants who consumed peanuts. Using whole-genome sequencing data, we performed a genome-wide association study (GWAS) for psIgG4 in the LEAP peanut consumption group participants (N = 267). We generated a cumulative genetic score from the identified loci and evaluated its association with psIgG4 levels in LEAP. The association was then assessed for replication in two independent peanut oral immunotherapy (PnOIT) trials, IMPACT and POISED. We identified 45 variants that reached suggestive significance (p < 1 × 10^-5), mapping to 17 independent loci in the LEAP peanut consumption group; none of these variants were associated with the psIgG4 levels in the avoidance group, highlighting a potential gene-by-environment (GxE) interaction. One locus on chromosome 2 showed regulatory signatures for SEPT2, a gene involved in epithelial barrier function. The genetic score was significantly associated with psIgG4 among LEAP consumers (β = 0.433; p = 1.20 × 10^-58) in the discovery cohort and IMPACT PnOIT participants (β = 0.287; p = 0.02) in an independent testing cohort. No association was observed in older POISED PnOIT participants (β = -0.029; p = 0.79). Identification of the SEPT2 locus in participants protected from peanut allergy (PA) suggests involvement of epithelial barrier pathways in modulating immune responses. Findings across all three trials emphasise the importance of GxE interactions, specifically the interplay between genetics and oral peanut exposure. Taken together, the findings indicate that early, sustained peanut consumption, combined with genetic factors, promotes a protective immune response to peanut allergens. Trial Registration: LEAP: NCT00329784; IMPACT: NCT03345160; POISED, NCT02103270.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"280-292"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146085589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Gut Ecosystem: Mechanism Studies From the Gut Microbiota to Inflammatory Cytokines to Inflammatory Bowel Disease.","authors":"Binbin Tang, Weixiang Cheng, Ajun Gu, Yangde Miao, Guang Yu, Jun Chen","doi":"10.1111/imm.70114","DOIUrl":"10.1111/imm.70114","url":null,"abstract":"<p><p>A potential association exists among gut microbiota, inflammatory mediators and inflammatory bowel disease (IBD), yet the precise biological mechanisms underlying these interconnections remain to be fully elucidated. Single nucleotide polymorphisms (SNPs) associated with gut microbiota were collected from the MiBioGen consortium. SNPs associated with IBD were sourced from GWAS research. Furthermore, a two-step MR approach was employed to clarify the potential mediating role of inflammatory factors in the causal relationship between gut microbiota and IBD. The genus Eubacterium ruminantium group (odds ratio [OR] = 1.087, 95% confidence interval [CI], 1.006-1.174, p = 0.035), genus Lachnospiraceae FCS020 group (OR, 1.172, 95% CI, 1.035-1.326, p = 0.012) were identified as a risk factor for IBD. Conversely, the family Bifidobacteriaceae performed a suggestively positive impact on the protective role against IBD (OR, 0.834, 95% CI, 0.728-0.956; p = 0.009), as well as family Clostridiaceae1 (OR, 0.827, 95% CI, 0.710-0.965; p = 0.016), family Lactobacillaceae (OR, 0.889, 95% CI, 0.798-0.991; p = 0.033) were found to be protective factors. Furthermore, our study indicated that the genus Lachnospiraceae FCS020 group contributed to the risk of IBD by affecting Interleukin-18 (IL-18), a mediation effect (OR = 1.015, 95% CI, 1.000-1.037, mediation proportion = 9.494%). This study offers genetic evidence from the perspective of bioinformatics to support potential causal mechanisms linking gut microbiota and IBD. Furthermore, from the perspective of gene prediction, it revealed the mediating role of IL-18 in the pathogenicity of the gut microbiota on IBD.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"269-279"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146085656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"STAT2 Mediated Epigenetic and Epitranscriptomic Regulation of CD4 ⁺ T Helper Cell Differentiation in Non-Small Cell Lung Cancer (NSCLC).","authors":"Roshni Bibi, Melvin George, Koustav Sarkar","doi":"10.1111/imm.70121","DOIUrl":"10.1111/imm.70121","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) is an aggressive malignancy necessitating innovative therapeutic approaches to augment antitumour immunity. Our study examined the function of the STAT2 protein in CD4⁺ T helper cells, which are essential for the immune response to cancer. We utilised CRISPR/Cas9 to ablate STAT2 in CD4⁺ T cells from stage I NSCLC patients (n = 30), assessing its impact on cellular function and diverse epigenetic pathways. Our findings indicate that the depletion of STAT2 markedly enhances the anti-cancer efficacy of T lymphocytes. Deletion of STAT2 diminished oxidative stress, enhanced the synthesis of advantageous TH1 cytokines. STAT2 depletion reduced DNA methylation and R-loop formation. T cells deficient in STAT2 showed enhanced efficacy in activating cytotoxic T lymphocytes to eliminate cancer cells. These findings identify STAT2 as a crucial regulator of immune function in the lung cancer microenvironment. Targeted STAT2 inhibition in tumour-reactive T cells may reinstate anti-tumour immunity, although systemic inhibition requires further research on targeted intervention strategies.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"293-306"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HIF1α Activates Glycolysis to Suppress Mycobacterium tuberculosis Growth in Mouse Bone Marrow-Derived Macrophages.","authors":"Junghwan Lee, Jaewhan Kim, Ji-Ae Choi, Tam Doan Nguyen, Seoyeon Jo, Chang-Hwa Song","doi":"10.1111/imm.70116","DOIUrl":"10.1111/imm.70116","url":null,"abstract":"<p><p>Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), remains a significant global health challenge due to the pathogen's ability to evade host immune responses and persist within macrophages. We investigated the metabolic changes in mouse bone marrow-derived macrophages (BMDMs) upon Mtb infection and identified significant alterations in gene expression related to key metabolic pathways through RNA sequencing analyses. Among them, glycolysis-related genes, including hypoxia-inducible factor 1α as a key regulator of glycolysis, are upregulated in Mtb-infected BMDMs. To investigate whether glycolysis plays a critical role in reducing intracellular Mtb growth, we cultured Mtb-infected BMDMs under high- or low-glucose conditions. We found that high-glucose conditions increased glycolytic enzyme levels, inducible nitric oxide synthase expression and proinflammatory cytokine production, reducing Mtb's intracellular survival. HIF1α agonist treatment increased glycolysis, reactive oxygen species levels and proinflammatory cytokine production, enhancing bactericidal activity against Mtb. In contrast, inhibition of HIF1α by a specific inhibitor FM19G11 leads to decreased glycolysis, reduced proinflammatory cytokine production and increased Mtb survival. Since succinate has been known to increase the stabilisation and activation of HIF1α, we added succinate to Mtb-infected BMDMs to evaluate the function of succinate related to HIF1α activation. As expected, succinate treatment enhanced glycolysis through HIF1α stabilisation and shifted BMDMs to proinflammatory M1-like phenotype. Our findings indicate that Mtb-induced glycolysis plays a central role in the reduction of intracellular Mtb in BMDMs. Succinate is a key factor for HIF1α-mediated glycolysis in Mtb-infected BMDMs.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"348-362"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146142293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum to \"New Role of Gramicidin A in RIG-I-Like Receptors-Mediated IFN Signalling\".","authors":"","doi":"10.1111/imm.70136","DOIUrl":"10.1111/imm.70136","url":null,"abstract":"","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"375"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Latent Neoehrlichia mikurensis Infections May Be Reactivated in Patients With B-Cell Lymphomas Treated With Rituximab.","authors":"Linda Wass, Catharina Lewerin, Daniel Jaén-Luchoro, Christine Lingblom, Christine Wennerås","doi":"10.1111/imm.70120","DOIUrl":"10.1111/imm.70120","url":null,"abstract":"<p><p>The intracellular, tick-borne bacterium Neoehrlichia (N.) mikurensis can cause neoehrlichiosis in patients with compromised B-cell defences, while immunocompetent individuals are frequently healthy carriers of the infection. We hypothesised that N. mikurensis induces latent infections that reactivate when B-cell immunity is compromised. We tested this hypothesis by determining the incidence of N. mikurensis reactivation in 97 patients with B-cell lymphomas who were treated with anti-CD20 antibody therapy (rituximab) and evaluating the presence of N. mikurensis-specific T cells in latently infected individuals. Four patients (4%) reactivated N. mikurensis infection and four patients (4%) had asymptomatic infection before the initiation of B-cell suppression. All eight patients who were infected with N. mikurensis had N. mikurensis-specific, perforin-expressing Th1 and CD8+ T-cell populations with up-regulation of CXCL10 and IFN-γ, in contrast to the noninfected lymphoma patients who lacked these T-cell subsets. The infected lymphoma patients also had expanded γδ T-cell populations. This study supports the notion of latent, reactivatable N. mikurensis infections.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"307-317"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial DNA: A Key Alarmin Igniting the Inflammasome Fire in Health and Disease.","authors":"Woo Hyun Park","doi":"10.1111/imm.70111","DOIUrl":"10.1111/imm.70111","url":null,"abstract":"<p><p>Beyond their classical role as cellular powerhouses, mitochondria are now recognised as indispensable hubs for innate immune signalling. A pivotal aspect of this function is the release of mitochondrial DNA (mtDNA), a potent damage-associated molecular pattern (DAMP) that, when misplaced, acts as a powerful alarmin due to its prokaryotic origins. In response to cellular stress or infection, mtDNA translocates to the cytosol and activates intracellular protein platforms known as inflammasomes, triggering the maturation of cytokines like interleukin-1β (IL-1β) and inducing a lytic form of cell death, pyroptosis. This review synthesises current research on this intricate relationship. Whilst potassium (K⁺) efflux remains the canonical trigger for the NLR family pyrin domain containing 3 (NLRP3) inflammasome, emerging and debated roles of oxidised mtDNA (ox-mtDNA) as a potential direct ligand or critical upstream amplifier are explored. The manuscript elucidates mtDNA release mechanisms, such as mitochondrial permeability transition pore (mPTP) opening, and explores the role of amplifying pathways like the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) axis and cytidine/uridine monophosphate kinase 2 (CMPK2)-mediated mtDNA synthesis. The profound involvement of the mtDNA-inflammasome axis is surveyed across a spectrum of pathologies, including autoimmune, metabolic, neurodegenerative, and cardiovascular diseases. The compiled evidence establishes mtDNA as a universal trigger of inflammation and a unifying pathogenic driver across this diverse disease landscape, highlighting the significant therapeutic potential of modulating this fundamental immune signalling axis to treat a multitude of human diseases.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"218-230"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146085594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of the Lectin Pathway Drives Persistent Complement Dysregulation in Long COVID.","authors":"Samuel B K Keat, Priyanka Khatri, Youssif M Ali, Chanuka H Arachchilage, Gregory Demopulos, Kirsten Baillie, Kelly L Miners, Kristin Ladell, Samantha A Jones, Helen E Davies, David A Price, Wioleta M Zelek, B Paul Morgan, Wilhelm J Schwaeble, Nicholas J Lynch","doi":"10.1111/imm.70110","DOIUrl":"10.1111/imm.70110","url":null,"abstract":"<p><p>Long COVID affects a substantial proportion of survivors of acute infection with severe acute respiratory syndrome-associated coronavirus-2 (SARS-CoV-2), who suffer a variety of symptoms that limit their quality of life and economic activity. Although the aetiology of long COVID is obscure, it appears to be a chronic inflammatory condition. Complement dysregulation is a prevalent feature of long COVID. Specifically, markers of classical, alternative, and terminal pathway activation are often elevated in patients with this condition. Here, we used a sensitive assay for mannan-binding lectin-associated serine protease-2 (MASP-2)/C1Inh complexes to analyse lectin pathway activation in a previously characterised cohort of patients with long COVID (n = 159) and healthy convalescent individuals with no persistent symptoms after infection with SARS-CoV-2 (n = 76). The data were combined with those from the most predictive complement analytes identified previously to delineate potential biomarkers of long COVID. MASP-2/C1Inh complexes were significantly elevated in patients with long COVID (p = 0.0003). Generalised linear modelling further identified an optimal set of four markers, namely iC3b (alternative pathway), TCC (terminal pathway), MASP-2/C1Inh (lectin pathway), and the complement regulator properdin, which had a receiver operating characteristic predictive power of 0.796 (95% confidence interval = 0.664-0.905). Combinations of the classical pathway markers C4, C1q, and C1s/C1Inh were poorly predictive of long COVID. These findings demonstrate that activation of the lectin complement pathway, which occurs upstream of the alternative and terminal pathways and can be inhibited therapeutically, is a salient feature of long COVID.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"261-268"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TREM-1 Blockade Inhibits Inflammasome Activation and Pyroptosis: Novel Insights on the Role of TREM-1 and Syk in Monosodium Urate Crystal-Induced Inflammation.","authors":"Yair Molad, Irina Lagovsky, Vitaly Kliminski","doi":"10.1111/imm.70108","DOIUrl":"10.1111/imm.70108","url":null,"abstract":"<p><p>Gout is associated with the upregulation of triggering receptor expressed on myeloid cells-1 (TREM-1) and soluble TREM-1 (sTREM-1). Cell activation signalling induced by monosodium urate (MSU) crystals and TREM-1 signalling both converge on spleen tyrosine kinase (Syk). The aim of this study was to decipher the role of the TREM-1 peptidomimetic inhibitor LP17, as well as Syk inhibitor, and their interaction during MSU-induced cell inflammation, focusing on NLRP3 inflammasome activation, IL-1β production and pyroptosis. In MSU-activated cells, both LP17 and Syk inhibitor (iSyk) significantly reduced the secretion of IL-1β and the release and activity of caspase-1. LP17 changed the phosphorylation of Syk, indicating that inhibition of TREM-1 modulates the activation state of Syk. Both LP17 and iSyk reduced the level of NLRP3-induced apoptosis-associated speck-like protein (ASC) transcripts and MSU-induced immunolabelling of ASC. Under confocal immunomicroscopy, TREM-1 in MSU-crystal-activated cells was localised to the same perimembranal compartment with NLRP3 inflammasome; inhibition of TREM-1 hindered the colocalisation of Syk with ASC. These results were corroborated by use of the in vitro ASC oligomerszation assay that showed that blocking TREM-1 induced Syk redistribution from ASC complexes, indicating that LP17 can repress the ability of Syk to incorporate into the forming ASC speckle. Additionally, unlike iSyk, LP17 hampered MSU-induced cleavage of gasdermin D, the hallmark of pyroptosis. Together, our findings suggest that blocking TREM-1 may prove beneficial as a novel strategy in the treatment of gout as well as other inflammasome-mediated diseases.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":"249-260"},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}