Immunology letters最新文献

Long-term monocyte activation after coronary artery bypass grafting: an exploratory prospective observational study. 冠状动脉旁路移植术后的长期单核细胞活化：一项探索性前瞻性观察研究。

IF 3.3 4区医学

Immunology letters Pub Date : 2024-11-01 DOI: 10.1016/j.imlet.2024.106941

Wieteke Broeders, Julia van Tuijl, Harmke B Duindam, Annemieke M Peters van Ton, Marlies P Noz, Peter Pickkers, Wilson F Abdo, Mihai G Netea, Siroon Bekkering, Niels P Riksen

{"title":"Long-term monocyte activation after coronary artery bypass grafting: an exploratory prospective observational study.","authors":"Wieteke Broeders, Julia van Tuijl, Harmke B Duindam, Annemieke M Peters van Ton, Marlies P Noz, Peter Pickkers, Wilson F Abdo, Mihai G Netea, Siroon Bekkering, Niels P Riksen","doi":"10.1016/j.imlet.2024.106941","DOIUrl":"https://doi.org/10.1016/j.imlet.2024.106941","url":null,"abstract":"<p><p>Major surgery such as coronary artery bypass grafting (CABG) is associated with an increased post-operative risk of atherosclerotic cardiovascular events. Cells of the innate immune system can adopt a long-lasting pro-inflammatory and atherogenic phenotype after brief exposure to exogenous or endogenous inflammatory stimuli, a process called \"trained immunity\". We hypothesized that the surgery-induced inflammation leads to sustained alterations in monocyte function, which promote the subsequent occurrence of cardiovascular events. Blood from 13 patients undergoing elective CABG was obtained before, 3-7 days (median 4) after, and 6-8 weeks (median 6) weeks after surgery. At 3-7 days postoperatively, circulating C-reactive protein (CRP) concentration, leukocyte counts and ex vivo Peripheral Blood Mononuclear Cell (PBMC) IL-6, TNFα and IL-1Ra production after stimulation (with various inflammatory stimuli) were significantly increased. Simultaneously, there was a reduction in monocyte HLA-DR expression. 6-8 weeks after CABG there was an ongoing systemic pro-inflammatory state with higher CRP concentrations, increased stimulated ex vivo PBMC IL-6 production, changes in monocytes subsets, and a higher expression of CCR2 on monocytes compared to baseline. In conclusion, CABG induces a persistent systemic inflammatory reaction with a sustained activated monocyte phenotype. This might contribute to the increased atherosclerotic cardiovascular event risk observed in cardiac surgery patients.</p>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142568200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

T cell landscape in the microenvironment of human solid tumors 人类实体瘤微环境中的 T 细胞图谱。

IF 3.3 4区医学

Immunology letters Pub Date : 2024-10-31 DOI: 10.1016/j.imlet.2024.106942

{"title":"T cell landscape in the microenvironment of human solid tumors","authors":"","doi":"10.1016/j.imlet.2024.106942","DOIUrl":"10.1016/j.imlet.2024.106942","url":null,"abstract":"<div><div>T cells are the main effectors involved in anti-tumor immunity, mediating most of the adaptive response towards cancer. After priming in lymph nodes, tumor antigens-specific naïve T lymphocytes proliferate and differentiate into effector CD4+ and CD8+ T cells that migrate from periphery into tumor sites aiming to eliminate cancer cells. Then while most effector T cells die, a small fraction persists and recirculates as long-lived memory T cells which generate enhanced immune responses when re-encountering the same antigen. A number of T (and non-T) cell subsets, stably resides in non-lymphoid peripheral tissues and may provide rapid immune response independently of T cells recruited from blood, against the reemergence of cancer cells. When tumor grows, however, tumor cells have evaded immune surveillance of effector cells (NK and CTL cells) which are exhausted, thus favoring the local expansion of T (and non-T) regulatory cells.</div><div>In this review, the current knowledge of features of T cells present in the tumor microenvironment (TME) of solid adult and pediatric tumors, the mechanisms upregulating immune-checkpoint molecules and transcriptional and epigenetic landscapes leading to dysfunction and exhaustion of T effector cells are reviewed. The interaction of T cells with cancer- or TME non-neoplastic cells and their secreted molecules shape the T cell profile compromising the intrinsic plasticity of T cells and, therefore, favoring immune evasion. In this phase regulatory T cells contribute to maintain a high immunosuppressive TME thus facilitating tumor cell proliferation and metastatic spread. Despite the advancements of cancer immunotherapy, many tumors are unresponsive to immune checkpoint inhibitors, or therapeutical vaccines or CAR T cell-based adoptive therapy: some novel strategies to improve these T cell-based treatments are lastly proposed.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142564380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The effect of abnormal lipid metabolism on immunosenescence of the colonic lamina propria in mice of different ages. 脂质代谢异常对不同年龄小鼠结肠固有层免疫衰老的影响

IF 3.3 4区医学

Immunology letters Pub Date : 2024-10-28 DOI: 10.1016/j.imlet.2024.106940

Fangyuan Cong, Yang Zhang, Jun Xu, Xiaohui Fang, Xia Li, Qian Xue, Jingtong Wang, Yulan Liu

{"title":"The effect of abnormal lipid metabolism on immunosenescence of the colonic lamina propria in mice of different ages.","authors":"Fangyuan Cong, Yang Zhang, Jun Xu, Xiaohui Fang, Xia Li, Qian Xue, Jingtong Wang, Yulan Liu","doi":"10.1016/j.imlet.2024.106940","DOIUrl":"https://doi.org/10.1016/j.imlet.2024.106940","url":null,"abstract":"<p><p>Immunosenescence is an age-associated change in immunological function. The intestinal mucosal immune system is considered the largest immune system in the human body, and its immunosenescence is closely related to the occurrence and development of many diseases. In recent years, studies have identified a crucial correlation between abnormal lipid metabolism induced by high-fat diet (HFD) and immunity, but the effect and mechanism of HFD on colonic mucosal immunosenescence are still unclear. In this study, we established an abnormal lipid metabolism model at different ages by feeding male wild-type mice HFD and compared the immunosenescence of the spleen, which reflects systemic immunity, and the colonic lamina propria (LP), which reflects local immunity. The results showed that HFD could lead to abnormal lipid metabolism at different ages, accelerate systemic and local immunosenescence, and increase the expression of inflammatory factors in colonic tissue. The levels of abnormal biochemical indicators induced by HFD were closely related to the proportions of T cell subsets associated with immunosenescence. Overall, the results showed that HFD had the most significant impact on aged mice. This study provides new ideas for further understanding the relationship between abnormal lipid metabolism and intestinal mucosal immunosenescence.</p>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142545263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Could tolerance to DNA be broken in the gut in systemic lupus erythematosus? 系统性红斑狼疮患者的肠道是否会破坏对 DNA 的耐受性？

IF 3.3 4区医学

Immunology letters Pub Date : 2024-10-28 DOI: 10.1016/j.imlet.2024.106937

{"title":"Could tolerance to DNA be broken in the gut in systemic lupus erythematosus?","authors":"","doi":"10.1016/j.imlet.2024.106937","DOIUrl":"10.1016/j.imlet.2024.106937","url":null,"abstract":"<div><div>The bacteria in the human colon outnumber the total number of nucleated cells in the human body by approximately 10:1. The DNA that the bacteria contain is enriched around 20-fold in immune stimulatory CpG motifs compared to the DNA of host cells. In addition, this DNA can have alternative more immunogeneic DNA structures and it may be presented to the immune system alongside other proinflammatory bacterial innate ligands such as LPS. To ensure that this immunostimulatory combination is not pathogenic, the luminal boundary of host tissues in the human gastrointestinal tract is protected by cells secreting bactericides together with the secreted enzyme DNASE1L3 that can break down bacterial DNA. Cells with RNA encoding DNASE1L3 are particularly abundant in the gut-associated lymphoid tissue where bacteria are specifically sampled into the body, alongside B cells noted for their T independent function. Importantly, individuals with loss of function mutations in DNASE1L3 develop anti-DNA antibodies and lupus symptoms.</div><div>In this review, we explore the possibility that a perfect storm might break tolerance to DNA: when bacterial DNA from microbiota that is not digested by DNASE1L3 directly encounters B cells that are not necessarily restricted by T cell dependence.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The importance of type I interferon in orchestrating the cytotoxic T-cell response to cancer I 型干扰素在协调细胞毒性 T 细胞对癌症的反应中的重要性

IF 3.3 4区医学

Immunology letters Pub Date : 2024-10-28 DOI: 10.1016/j.imlet.2024.106938

{"title":"The importance of type I interferon in orchestrating the cytotoxic T-cell response to cancer","authors":"","doi":"10.1016/j.imlet.2024.106938","DOIUrl":"10.1016/j.imlet.2024.106938","url":null,"abstract":"<div><div>Both type I interferon (IFN-I) and CD4<sup>+</sup> T-cell help are required to generate effective CD8<sup>+</sup> T-cell responses to cancer. We here outline based on existing literature how IFN-I signaling and CD4<sup>+</sup> T-cell help are connected. Both impact on the functional state of dendritic cells (DCs), particularly conventional (c)DC1. The cDC1s are critical for crosspresentation of cell-associated antigens and for delivery of CD4<sup>+</sup> T-cell help for cytotoxic T-lymphocyte (CTL) effector and memory differentiation. In infection, production of IFN-I is prompted by pathogen-associated molecular patterns (PAMPs), while in cancer it relies on danger-associated molecular patterns (DAMPs). IFN-I production by tumor cells and pDCs in the tumor micro-environment (TME) is often limited. IFN-I signals increase the ability of migratory cDC1s and cDC2s to transport tumor antigens to tumor-draining lymph nodes (tdLNs). IFN-I also enables cDC1s to form and sustain the platform for help delivery by stimulating the production of chemokines that attract CD4<sup>+</sup> and CD8<sup>+</sup> T cells. IFN-I promotes delivery of help in concert with CD40 signals by additive and synergistic impact on cross-presentation and provision of critical costimulatory and cytokine signals for CTL effector and memory differentiation. The scenario of CD4<sup>+</sup> T-cell help therefore depends on IFN-I signaling. This scenario can play out in tdLNs as well as in the TME, thereby contributing to the cancer immunity cycle. The collective observations may explain why both IFN-I and CD4<sup>+</sup> T-cell help signatures in the TME correlate with good prognosis and response to PD-1 targeting immunotherapy in human cancer. They also may explain why a variety of tumor types in which IFN-I signaling is attenuated, remain devoid of functional CTLs.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142560883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Study of the mechanism of fibroblast-like synoviocytes-derived exosomes inducing macrophages M1 polarization and CD8⁺T cells immune regulation ferroptosis and autophagy in rheumatoid arthritis. 成纤维细胞样滑膜细胞外泌体诱导类风湿性关节炎巨噬细胞M1极化和CD8+T细胞免疫调节铁蛋白沉积及自噬的机制研究

IF 3.3 4区医学

Immunology letters Pub Date : 2024-10-22 DOI: 10.1016/j.imlet.2024.106936

Fang Fang, Mengqing Hua, GenMing Yu

{"title":"Study of the mechanism of fibroblast-like synoviocytes-derived exosomes inducing macrophages M1 polarization and CD8<sup>+</sup>T cells immune regulation ferroptosis and autophagy in rheumatoid arthritis.","authors":"Fang Fang, Mengqing Hua, GenMing Yu","doi":"10.1016/j.imlet.2024.106936","DOIUrl":"https://doi.org/10.1016/j.imlet.2024.106936","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a chronic autoimmune disease that affects the joints. The pathogenesis of RA is complex, involving membrane lipid antioxidant systems, oxidative stress, and lipid peroxidation. In this study, it was found that cysteine dioxygenase 1 (CDO1) is significantly upregulated in RA fibroblast-like synoviocytes (RA-FLS) and that exosomes derived from these RA-FLS deliver CDO1 to promote M1 polarization of macrophages, thus facilitating RA progression. In the immune microenvironment, CD8<sup>+</sup>T cells play a role in immune regulation by producing cytokines such as interferon gamma (IFNγ) in various diseases. The results of this study suggested that in RA-FLS, CD8<sup>+</sup>T cells deliver IFNγ, which not only inhibits the viability of RA-FLS but also affects glutathione (GSH) through CDO1, regulating the GPX4 antioxidant signaling pathway to promote ferroptosis and autophagy in cells. It was also discovered that IFNγ enhances the expression of TRI69, ubiquitinates and degrades FSP1, thereby forming a cooperative regulation process of GPX4 and FSP1 in ferroptosis. These findings provide a new direction for the treatment of RA.</p>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fingolimod, an antagonist of sphingosine 1-phosphate, ameliorates Sjögren's syndrome by reducing the number of STAT3–induced germinal center B cells and increasing the number of Breg cells 鞘氨醇1-磷酸拮抗剂芬戈莫德可通过减少STAT3诱导的生殖中心B细胞数量和增加Breg细胞数量来改善Sjögren综合征。

IF 3.3 4区医学

Immunology letters Pub Date : 2024-10-11 DOI: 10.1016/j.imlet.2024.106935

{"title":"Fingolimod, an antagonist of sphingosine 1-phosphate, ameliorates Sjögren's syndrome by reducing the number of STAT3–induced germinal center B cells and increasing the number of Breg cells","authors":"","doi":"10.1016/j.imlet.2024.106935","DOIUrl":"10.1016/j.imlet.2024.106935","url":null,"abstract":"<div><h3>Background</h3><div>Sjögren's syndrome (SS) is an autoimmune disease caused by infiltrating lymphocytes. FTY720 affects the S1P signaling pathway, which plays a role in T and B cell migration from secondary lymphoid tissues to target organs. In this study, we investigate the regulatory mechanism of FTY720 in the context of SS.</div></div><div><h3>Method</h3><div>FTY720 was given orally every day to NOD mice. The salivary flow rate (SFR) and blood glucose level were assayed every 3 weeks. Histopathological features were investigated at the end of the study. In vitro, FTY720 was added to mouse splenocytes, and changes in the lymphocyte subsets were assessed.</div></div><div><h3>Results</h3><div>In vivo, FTY720 increased the SFR and reduced the blood glucose level. The salivary gland histological score and infiltration of the salivary glands by B and T cells were dramatically decreased. Furthermore, STAT expression in the salivary gland was decreased. In vitro, FTY720 inhibited Th17 cells, while increasing regulatory T (Treg) cells, respectively. Also, FTY720 decreased and increased the numbers of germinal center (GC) B cells and regulatory B cells (Breg cells), respectively. FTY720 decreased the IgG level in culture supernatants. Also, STAT3 activation was decreased by FTY720.</div></div><div><h3>Conclusion</h3><div>Our results show the therapeutic potential of FTY720 in the context of SS; FTY720 prevents lymphocyte migration from secondary lymphoid organs to target organs.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ursolic acid attenuates pseudo-allergic reactions via reducing MRGPRX2-mediated mast cell degranulation 熊果酸通过减少 MRGPRX2 介导的肥大细胞脱颗粒来减轻假性过敏反应

IF 3.3 4区医学

Immunology letters Pub Date : 2024-10-10 DOI: 10.1016/j.imlet.2024.106934

{"title":"Ursolic acid attenuates pseudo-allergic reactions via reducing MRGPRX2-mediated mast cell degranulation","authors":"","doi":"10.1016/j.imlet.2024.106934","DOIUrl":"10.1016/j.imlet.2024.106934","url":null,"abstract":"<div><div>Mas-related G protein–coupled receptor X2 (MRGPRX2) is a newly identified receptor on mast cells that contribute to IgE-independent pseudo-allergy. Ursolic acid (UA), a pentacyclic triterpenoid, has been reported for its anti-allergy effects. However, the protective mechanism against pseudo-allergic reactions remains unclear. This study aims to investigate the effects of UA on pseudo-allergic reactions both <em>in vivo</em> and <em>in vitro</em>, focusing on the therapeutical mechanism underlying its effect on mast cells. In present study, UA reduced degranulation and chemokines production induced by MRGPRX2 agonists, including compound 48/80 (C48/80) and substance P (SP), in LAD2 cells <em>in vitro</em>. UA also alleviated C48/80 and SP-induced systemic anaphylaxis and passive cutaneous anaphylaxis (PCA) <em>in vivo</em>. Furthermore, UA demonstrated strong binding affinity to the MRGPRX2 protein, leading to a decrease in calcium influx in both LAD2 cells and MRGPRX2-HEK293 cells stimulated with C48/80 and SP. Moreover, UA effectively suppressed phosphorylation levels within phospholipase C-γ (PLCγ) pathway and nuclear factor kappa-B (NF-κB) pathway of MRGPRX2 downstream proteins. Our findings indicated that UA exerts an attenuating effect in pseudo-allergic reactions by suppressing MRGPRX2-mediated mast cell activation, targeting PLCγ pathway and NF-κB pathway. These results suggest that UA may serve as a promising therapeutic agent for MRGPRX2-dependent pseudo-allergic reactions.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142441805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of neutrophils in ANCA-associated vasculitis 中性粒细胞在 ANCA 相关性血管炎中的作用

IF 3.3 4区医学

Immunology letters Pub Date : 2024-10-01 DOI: 10.1016/j.imlet.2024.106933

引用次数: 0

Fighting the enemy within: Systemic immune defense against mucosal Salmonella infection 与内部敌人作战：针对粘膜沙门氏菌感染的全身免疫防御。

IF 3.3 4区医学

Immunology letters Pub Date : 2024-09-27 DOI: 10.1016/j.imlet.2024.106930

{"title":"Fighting the enemy within: Systemic immune defense against mucosal Salmonella infection","authors":"","doi":"10.1016/j.imlet.2024.106930","DOIUrl":"10.1016/j.imlet.2024.106930","url":null,"abstract":"<div><div><em>Salmonella</em> infection remains a persistent global health threat, as different serovars induce a range of clinical disease, depending upon bacterial virulence and host susceptibility. While some <em>Salmonella</em> serovars induce gastroenteritis in healthy individuals, others can cause more serious systemic enteric fever or invasive nontyphoidal Salmonellosis. The rise of antibiotic resistance, coupled with the absence of effective vaccines for most serovars, perpetuates the spread of <em>Salmonella</em> in endemic regions. A detailed mechanistic understanding of immunity to <em>Salmonella</em> infections has been aided by the availability of mouse models that have served as a valuable tool for understanding host-pathogen interactions under controlled laboratory conditions. These mouse studies have delineated the processes by which early inflammation is triggered after infection, how adaptive immunity is initiated in lymphoid tissues, and the contribution of lymphocyte memory responses to resistance. While recent progress has been made in vaccine development for some causes of enteric fever, deeper understanding of <em>Salmonella</em>-specific immune memory might allow the formation of new vaccines for all serovars. This review will provide a summary of our understanding of vaccination and protective immunity to <em>Salmonella</em> with a focus on recent developments in T cell memory formation.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0