Journal of Experimental Medicine最新文献

Complement-regulated homeostatic proliferation controls memory B cell longevity and repertoire composition. 补体调节的稳态增殖控制记忆B细胞寿命和曲目组成。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-07-06 Epub Date: 2026-05-08 DOI: 10.1084/jem.20251048

Evan W Cody, Mehek Ningoo, Isha Monga, Alexander M Tsankov, Hiromi Muramatsu, Norbert Pardi, Miguel Fribourg, Peter S Heeger, David Dominguez-Sola

{"title":"Complement-regulated homeostatic proliferation controls memory B cell longevity and repertoire composition.","authors":"Evan W Cody, Mehek Ningoo, Isha Monga, Alexander M Tsankov, Hiromi Muramatsu, Norbert Pardi, Miguel Fribourg, Peter S Heeger, David Dominguez-Sola","doi":"10.1084/jem.20251048","DOIUrl":"https://doi.org/10.1084/jem.20251048","url":null,"abstract":"Memory B cell (Bmem) survival is essential for guarding against reinfection, yet processes ensuring their longevity remain unclear. As decay-accelerating factor (DAF, CD55), a negative regulator of complement activation, is requisitely downregulated on germinal center B cells and is reexpressed on Bmem, we investigated the effects of deleting DAF on murine (B1-8hi) Bmem in competitive settings. Kinetic analysis showed a progressive reduction in DAF-/- Bmem numbers over 6 wk, without affecting Bmem production, pool size, or their ability to respond to rechallenge. Following transfer into unimmunized hosts, wild-type Bmem proliferated to maintain stable Bmem pool sizes, outcompeting DAF-/- Bmem, reflecting homeostatic proliferation. Reduced proliferation and increased cell death in DAF-/- Bmem associated with transcriptional differences in metabolism and migration pathways. Wild-type Bmem proliferation increased in C3-/- hosts, and vaccination with a heterologous antigen, which induces local complement activation, locally inhibited bystander B1-8hi Bmem proliferation. Thus, complement-dependent regulation of Bmem homeostatic proliferation influences Bmem longevity and repertoire composition in mice.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"223 7","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

BACH2 controls ILC3 function via PPARγ-dependent mitochondrial metabolism. BACH2通过ppar γ依赖性线粒体代谢控制ILC3功能。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-06-01 Epub Date: 2026-04-28 DOI: 10.1084/jem.20251918

Jianye Wang, Ying Wang, Gaoyu Liu, Jinhao Yang, Houjia Hu, Hailong Cao, Shuo Wang, Xuanlin Liu, Jingyi Wu, Meng Yao, Xiaolei Pan, Pan Zhou, Ying Yu, Zuoqing Song, Qiang Liu, Jie Zhou

{"title":"BACH2 controls ILC3 function via PPARγ-dependent mitochondrial metabolism.","authors":"Jianye Wang, Ying Wang, Gaoyu Liu, Jinhao Yang, Houjia Hu, Hailong Cao, Shuo Wang, Xuanlin Liu, Jingyi Wu, Meng Yao, Xiaolei Pan, Pan Zhou, Ying Yu, Zuoqing Song, Qiang Liu, Jie Zhou","doi":"10.1084/jem.20251918","DOIUrl":"https://doi.org/10.1084/jem.20251918","url":null,"abstract":"Group 3 innate lymphoid cells (ILC3s) play an essential role in maintaining intestinal barrier immunity. Dysfunction of ILC3s contributes to the pathogenesis of inflammatory bowel disease (IBD), whereas the mechanisms underlying ILC3 regulation remain incompletely understood. Here, we report that the transcription factor BTB domain and CNC homolog 2 (BACH2) represents an important regulator of intestinal ILC3s. ILC3s from IBD patients exhibited reduced BACH2 expression compared with those from healthy donors. Conditional ablation of BACH2 in ILC3s impaired their function, thereby exacerbating the severity of murine colitis. Mechanistically, BACH2 enhanced mitochondrial oxidative phosphorylation in ILC3s in a peroxisome proliferator-activated receptor γ (PPARγ)-dependent manner. PPARγ was identified as a direct transcriptional target of BACH2 in ILC3s. Notably, pharmacological activation of PPARγ with rosiglitazone restored ILC3 function and ameliorated colitis in BACH2-deficient mice. These observations demonstrate that the presence of BACH2-PPARγ signaling in ILC3s protects against colitis.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"223 6","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

TACItness MZ B cell maturation. mzb细胞成熟。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-06-01 Epub Date: 2026-05-05 DOI: 10.1084/jem.20260401

Mauricio Guzmán, Martyna Filipska, Andrea Cerutti

引用次数: 0

Rab5 improves CAR T cell efficacy via reducing fratricide and maintaining surface CAR levels. Rab5通过减少杀兄弟性和维持表面CAR水平来提高CAR - T细胞的功效。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-06-01 Epub Date: 2026-05-05 DOI: 10.1084/jem.20252564

Meidi Gu, Kaitlin A Read, Vipin Bhardwaj, Edmund J Carvalho, David Nardo, Justin C Shayne, Divanshu Shukla, Wei Liu, Donald L Siegel, Neil C Sheppard, Michael C Milone, Adam D Cohen, Alfred L Garfall, James L Riley

{"title":"Rab5 improves CAR T cell efficacy via reducing fratricide and maintaining surface CAR levels.","authors":"Meidi Gu, Kaitlin A Read, Vipin Bhardwaj, Edmund J Carvalho, David Nardo, Justin C Shayne, Divanshu Shukla, Wei Liu, Donald L Siegel, Neil C Sheppard, Michael C Milone, Adam D Cohen, Alfred L Garfall, James L Riley","doi":"10.1084/jem.20252564","DOIUrl":"https://doi.org/10.1084/jem.20252564","url":null,"abstract":"We show continuous tumor exposure results in a loss of chimeric antigen receptor (CAR) T cell (CART) endocytic activity due to downregulation of Rab5. Loss of endocytic activity exacerbates the effects of trogocytosis, the bidirectional transfer of tumor target antigens and CARs between malignant cells and CARTs, resulting in CART dysfunction and fratricide. Constitutive expression of Rab5 within the CARTs reduced fratricide by reducing the amount of trogocytosed antigens on the cell surface, while simultaneously enhancing CAR availability through dissociation of CAR from target, recycling unbound CAR back to the plasma membrane, and limiting CAR capture by tumor cells. Rab5-expressing CARTs exhibited superior antitumor activity in both BCMA-CARTs isolated from the bone marrow of treated patients and mesothelin-specific CARTs in a solid tumor model. These studies uncover an unexpected relationship between endocytosis and CART function and suggest that pairing Rab5 with CAR expression could improve the clinical efficacy of CART therapy.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"223 6","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

B7 costimulation antagonizes RORγt+ regulatory T cells and immune tolerance in the intestine. B7共刺激拮抗r γ T +调节性T细胞和肠道免疫耐受。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-06-01 Epub Date: 2026-04-24 DOI: 10.1084/jem.20251094

Mengze Lyu, Gregory F Sonnenberg

{"title":"B7 costimulation antagonizes RORγt+ regulatory T cells and immune tolerance in the intestine.","authors":"Mengze Lyu, Gregory F Sonnenberg","doi":"10.1084/jem.20251094","DOIUrl":"https://doi.org/10.1084/jem.20251094","url":null,"abstract":"Regulatory T (Treg) cells that recognize dietary- or microbiota-derived antigens express RORγt and are essential for immune tolerance in the intestine. A recent paradigm shift found these cells require major histocompatibility complex class II (MHCII) on RORγt+ antigen-presenting cells (APCs) rather than conventional dendritic cells (cDCs) for signal one. Here, we evaluate signal two and unexpectedly find that costimulatory molecules B7-1 (CD80) and B7-2 (CD86) antagonize the generation of microbiota-specific RORγt+ Treg cells. Gain-of-function or loss-of-function therapeutics targeting B7 via CTLA-4 exert reciprocal effects on the generation of microbiota-specific RORγt+ Treg cells. This axis was independent of B7 on RORγt+ APCs but required MHCII on this cell type. Finally, CTLA4-Ig treatment restores microbiota-specific RORγt+ Treg cell generation and protects from experimental intestinal inflammation induced by pathobiont colonization with IL-10R signaling blockade. These results define that RORγt+ Treg cells are uniquely restrained by B7 costimulation, while CTLA4-Ig enhances immune tolerance in the intestine when acting cooperatively with RORγt+ APCs.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"223 6","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Tet2 deficiency alters CD4+ T cell function and promotes T cell lymphoma with a TFH cell immunophenotype. Tet2缺乏改变CD4+ T细胞功能并促进具有TFH细胞免疫表型的T细胞淋巴瘤。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-06-01 Epub Date: 2026-04-28 DOI: 10.1084/jem.20250194

Tayla B Heavican-Foral, Yuping Li, Waseem Lone, Alyssa Bouska, Jibin Zhang, Ruimeng Yang, Xuxiang Liu, Ab Rauf Shah, Abdul Rouf Mir, Joseph Rohr, Dylan Jochum, Anurag Kumar, Ravneet Singh Chawla, Catalina Amador, Jiayu Yu, Tyler Herek, Jacob Robinson, Chengfeng Bi, Sunandini Sharma, Tyler Gilbreath, R Katherine Hyde, Timothy W McKeithan, Chan-Wang Lio, Anjana Rao, Giorgio Inghirami, Joesph Khoury, Wing C Chan, Javeed Iqbal

{"title":"Tet2 deficiency alters CD4+ T cell function and promotes T cell lymphoma with a TFH cell immunophenotype.","authors":"Tayla B Heavican-Foral, Yuping Li, Waseem Lone, Alyssa Bouska, Jibin Zhang, Ruimeng Yang, Xuxiang Liu, Ab Rauf Shah, Abdul Rouf Mir, Joseph Rohr, Dylan Jochum, Anurag Kumar, Ravneet Singh Chawla, Catalina Amador, Jiayu Yu, Tyler Herek, Jacob Robinson, Chengfeng Bi, Sunandini Sharma, Tyler Gilbreath, R Katherine Hyde, Timothy W McKeithan, Chan-Wang Lio, Anjana Rao, Giorgio Inghirami, Joesph Khoury, Wing C Chan, Javeed Iqbal","doi":"10.1084/jem.20250194","DOIUrl":"10.1084/jem.20250194","url":null,"abstract":"TET2 mutations are frequent in TFH-derived lymphomas, but how epigenetic disruption initiates malignant T cell transformation is unclear. We generated Cd4cre;Tet2FL/FL mice, which developed aggressive T cell lymphoma (m-TCL) with a TFH cell-like immunophenotype. Genome-wide transcriptomics and epigenetic profiling of Tet2-/- CD4+ T cells prior to lymphoma development showed hyperactive TCR, PI3K signaling, and dysregulated TH differentiation program, with proliferation promoting signal transduction at the lymphoma stage. Tet2 loss promoted hyperplasticity under in vitro conditions but favored conditional TFH differentiation. Reduced 5-hmC levels at regulatory genomic elements, resulted in transcriptional rewiring of TFH-associated genes, promoting ICOS(L)-mediated PI3K signaling. TET2-KO human CD4+ T cells showed conserved epigenetic changes with increased proliferation, decreased exhaustion, increased memory marker expression, and clonal expansion with restricted TCR repertoire under in vitro conditions. scRNA-seq revealed a persistent proliferative cluster characterized by elevated stem-like transcriptional features compared with WT counterparts. Tet2-/- m-TCLs allografted into NSG mice showed a significant response to epigenetic (5-azacytidine) and PI3K inhibitors (duvelisib) alone or in combination.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"223 6","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Mesenteric macrophage-monocyte circuit controls systemic inflammation during enteric bacterial infection. 肠系膜巨噬细胞-单核细胞回路控制肠道细菌感染时的全身炎症。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-06-01 Epub Date: 2026-04-28 DOI: 10.1084/jem.20251492

Jiseon Kim, Joseph R Dominguez, Seung Hyeon Kim, Zachary White, Jaewon Cho, Jungmin Hwang, Yeonwoo Choi, Soroush Tahmasebi, Teruyuki Sano, Jinki Yeom, Ki-Wook Kim

{"title":"Mesenteric macrophage-monocyte circuit controls systemic inflammation during enteric bacterial infection.","authors":"Jiseon Kim, Joseph R Dominguez, Seung Hyeon Kim, Zachary White, Jaewon Cho, Jungmin Hwang, Yeonwoo Choi, Soroush Tahmasebi, Teruyuki Sano, Jinki Yeom, Ki-Wook Kim","doi":"10.1084/jem.20251492","DOIUrl":"https://doi.org/10.1084/jem.20251492","url":null,"abstract":"Although the gut mesentery is anatomically linked to the intestines, the roles of mesentery-resident macrophages and mesentery-recruited monocytes, particularly in gut inflammation, remain poorly defined. Here, we show that mesenteric macrophage-monocyte interactions limit systemic infection during Salmonella Typhimurium (STm)-induced gut inflammation. Using Ccr2-deficient mice and fate-mapping approaches, we identified two distinct granulocyte-monocyte progenitor (GMP)-derived macrophage populations in the gut mesentery, LYVE1hi TIM4(-) and LYVE1lo/- TIM4(-) subsets, alongside embryonically derived LYVE1hi TIM4(+) macrophages. LYVE1lo/- TIM4(-) macrophages, but not LYVE1hi macrophages, removed excessively recruited neutrophils during STm infection, whereas newly mesentery-recruited monocytes were the primary source of inflammatory cytokines. Moreover, depletion of mesentery-resident macrophages in mice lacking Csf1 in serous stromal cells resulted in excessive recruitment of GMP-derived monocytes accompanied by elevated expression of inflammatory cytokines, thereby accelerating mortality during STm infection. Together, our findings reveal that the mesenteric macrophage-monocyte circuit buffers the escalation of gut infection into systemic inflammation.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"223 6","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

TACI regulates marginal zone B cell development. TACI调节边缘区B细胞的发育。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-06-01 Epub Date: 2026-05-05 DOI: 10.1084/jem.20251308

Daisy H Luff, Lesley Vanes, Stefan Boeing, Victor L J Tybulewicz

引用次数: 0

Antibody-mediated diversification of primary and secondary humoral immune responses. 抗体介导的原发性和继发性体液免疫反应的多样化。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-06-01 Epub Date: 2026-04-28 DOI: 10.1084/jem.20252590

Dennis Schaefer-Babajew, Laurine Binet, Gabriela S Silva Santos, Chiara Ruprecht, Lachlan P Deimel, Mohamed A ElTanbouly, Dounia Gharrassi, Gabriella Lima Dos Reis, Clara Uhe, Kai-Hui Yao, Brianna Hernandez, Parul Agrawal, Anna Gazumyan, Leonidas Stamatatos, Harald Hartweger, Michel C Nussenzweig

{"title":"Antibody-mediated diversification of primary and secondary humoral immune responses.","authors":"Dennis Schaefer-Babajew, Laurine Binet, Gabriela S Silva Santos, Chiara Ruprecht, Lachlan P Deimel, Mohamed A ElTanbouly, Dounia Gharrassi, Gabriella Lima Dos Reis, Clara Uhe, Kai-Hui Yao, Brianna Hernandez, Parul Agrawal, Anna Gazumyan, Leonidas Stamatatos, Harald Hartweger, Michel C Nussenzweig","doi":"10.1084/jem.20252590","DOIUrl":"10.1084/jem.20252590","url":null,"abstract":"Humoral immune responses are characterized by increasing antibody affinity and diversity over time. Increased affinity is mediated by a combination of immunoglobulin gene somatic mutation and iterative cycles of selection in germinal centers. Less is understood about how diversity increases. Here, we examine the role of antibody feedback in diversifying immune responses in mice that produce B cells that are incapable of secreting antibodies. To this end, we produced two strains of mice, one that expresses only membrane and secreted forms of IgM, and a second that produces only the membrane-bound form of IgM. Analysis of primary and secondary immune responses shows that antibody feedback significantly diversifies both primary and secondary immune responses even when antibodies are present at levels that are 10-30-fold lower than physiologic. The data have significant implication for sequential vaccination approaches aimed at shepherding immunity to produce broadly neutralizing antibodies to highly diversified pathogens such as HIV-1 and influenza.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"223 6","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

AID and TET2 cooperate to demethylate Irf4 for plasma cell fate in germinal center B cells. AID和TET2协同Irf4去甲基化，影响生发中心B细胞浆细胞的命运。

IF 10.6 1区医学

Journal of Experimental Medicine Pub Date : 2026-06-01 Epub Date: 2026-04-27 DOI: 10.1084/jem.20260096

Minghui He, Roberta D'Aulerio, Lia G Pinho, Evangelos Doukoumopoulos, Tracer Yong, Rhaissa C Vieira, Mariana M S Oliveira, Laura Eiben, Manon Termote, Rômulo G Galvani, Saikiran Sedimbi, Christina Seitz, Nikolai V Kuznetsov, Maria A Zuriaga, Daisuke Kitamura, José J Fuster, Vinicius Cotta-de-Almeida, Lena Ström, Pia Dosenovic, Søren E Degn, Lisa S Westerberg

{"title":"AID and TET2 cooperate to demethylate Irf4 for plasma cell fate in germinal center B cells.","authors":"Minghui He, Roberta D'Aulerio, Lia G Pinho, Evangelos Doukoumopoulos, Tracer Yong, Rhaissa C Vieira, Mariana M S Oliveira, Laura Eiben, Manon Termote, Rômulo G Galvani, Saikiran Sedimbi, Christina Seitz, Nikolai V Kuznetsov, Maria A Zuriaga, Daisuke Kitamura, José J Fuster, Vinicius Cotta-de-Almeida, Lena Ström, Pia Dosenovic, Søren E Degn, Lisa S Westerberg","doi":"10.1084/jem.20260096","DOIUrl":"https://doi.org/10.1084/jem.20260096","url":null,"abstract":"Activation-induced cytidine deaminase (AID) is essential for B cell affinity maturation. We investigated why AID deficiency gives rise to giant germinal centers (GCs) using the AIDR112H mouse model that is devoid of AID activity. The increased GC response was associated with accumulation of GC B cells in the light zone in immunized AIDR112H mice. AIDR112H GC B cells had reduced capacity to upregulate IRF4 to initiate plasma cell differentiation, leading to accumulation of a transitional GC population with reduced GL7 expression. Genetic introduction of a high-affinity B cell receptor was unable to restore plasma cell differentiation of AIDR112H B cells, while ectopic expression of catalytically active AID rescued plasma cell generation. AID and ten-eleven translocation 2 (TET2) synergistically facilitated demethylation of the Irf4 promoter/enhancer, and this was impeded in AIDR112H cells. These data reveal a B cell-intrinsic mechanism that governs the plasma cell fate decision through epigenetic remodeling mediated by AID in cooperation with TET2.","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"223 6","pages":""},"PeriodicalIF":10.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13116153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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