ImmunoHorizons最新文献_第5页

SHIP-1 adapter functions mediate recruitment of FCRL1 to the BCR and inhibition of ERK. SHIP-1适配器功能介导FCRL1向BCR的募集和ERK的抑制。

ImmunoHorizons Pub Date : 2026-04-11 DOI: 10.1093/immhor/vlaf067

Malory M Wolfe, Rut Tallon Arranz, Elizabeth L Zenni, Timothy J Wilson

{"title":"SHIP-1 adapter functions mediate recruitment of FCRL1 to the BCR and inhibition of ERK.","authors":"Malory M Wolfe, Rut Tallon Arranz, Elizabeth L Zenni, Timothy J Wilson","doi":"10.1093/immhor/vlaf067","DOIUrl":"10.1093/immhor/vlaf067","url":null,"abstract":"FCRL1 is a plasma membrane coreceptor on B cells that has been shown to potentiate B cell receptor (BCR)-driven calcium flux and negatively regulate ERK phosphorylation in a GRB2 and tyrosine-dependent manner. Of the proteins that associate with FCRL1, the recruitment of the inositol phosphatase SHIP-1 is GRB2 dependent, implicating SHIP-1 in FCRL1-mediated ERK regulation. Using immunoprecipitation and Western blotting, it was found that a proline-rich region in the C-terminus of SHIP-1, rather than its N-terminal SH2 domain, mediates recruitment of SHIP-1 to Y281 in FCRL1 in a manner dependent on GRB2. Interestingly, Y281 and GRB2 were also required for FCRL1 colocalization to the BCR. Translational fusions between tyrosine-mutated FCRL1 and the SH2 domain of SHIP-1 were sufficient to drive both colocalization of FCRL1 with the BCR as well as the ERK-inhibitory activity of FCRL1. Our data are consistent with a function for SHIP-1 as an adapter between FCRL1 and the BCR signalosome, and that this adapter function is responsible for BCR/FCRL1 colocalization after BCR stimulation and modulation of ERK signaling.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13071153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147679101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Development of a flow cytometry method to measure antidrug antibodies against CAR T cells. 开发一种流式细胞术方法来测量抗CAR - T细胞的抗药物抗体。

ImmunoHorizons Pub Date : 2026-04-11 DOI: 10.1093/immhor/vlag011

Georgia Day, Francisco Javier Sánchez-Martín, Lisa Seavers, Karen Cadwallader, Sara Morgado-García

{"title":"Development of a flow cytometry method to measure antidrug antibodies against CAR T cells.","authors":"Georgia Day, Francisco Javier Sánchez-Martín, Lisa Seavers, Karen Cadwallader, Sara Morgado-García","doi":"10.1093/immhor/vlag011","DOIUrl":"10.1093/immhor/vlag011","url":null,"abstract":"Chimeric antigen receptor (CAR) T cell therapies are based on the genetic modification of the T cell receptor of a patient's own T cells. The resulting CAR T cells cytotoxic response is redirected against a specific tumor antigen. This innovative immunotherapy has been used successfully to treat blood malignancies, and it is also being developed as treatment for solid tumors. CAR T cells can lead to immune related adverse outcomes associated with an unwanted immune response in the host, ranging from acute events to those sustained with time, such as antidrug antibody (ADA) development, which can impact the efficacy and persistence of the CAR T cells once administered to the patient. The development of ADAs as response to a drug treatment is not exclusive to CAR T cells, and evidence of their production has been long acknowledged. While traditional types of analysis aim to measure the presence of ADAs by immunoassay methods, with the therapeutic agent being cells, the use of a flow cytometry approach has become the obvious choice for detection and quantification of ADAs against CAR T cells products, as well as any other cell therapies. Here, we present the results of the development of a flow cytometry method to measure ADAs using CAR T cells with an assay to detect the binding of an ADA-like molecule to the CAR T cells in a dose-dependent manner. This method allowed for quantification of ADAs and determination of the assay values needed for potential ADA measurement in clinical samples.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13109846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TGF-β-induced Tregs release extracellular vesicles that modulate CD4+ T-cell proliferation and phenotype in a Nrp1-dependent manner. TGF-β诱导的Tregs释放细胞外囊泡，以nrp1依赖的方式调节CD4+ t细胞增殖和表型。

ImmunoHorizons Pub Date : 2026-04-11 DOI: 10.1093/immhor/vlag019

María José Moya-Guzmán, Eduardo González-Mienert, Camila Pinto, Karina Pino-Lagos

{"title":"TGF-β-induced Tregs release extracellular vesicles that modulate CD4+ T-cell proliferation and phenotype in a Nrp1-dependent manner.","authors":"María José Moya-Guzmán, Eduardo González-Mienert, Camila Pinto, Karina Pino-Lagos","doi":"10.1093/immhor/vlag019","DOIUrl":"10.1093/immhor/vlag019","url":null,"abstract":"Neuropilin-1 (Nrp1) is one of the receptors for TGF-β and is associated with the suppressive function of T regulatory cells (Tregs). Based on previous findings on natural Tregs, this work investigated the role of Nrp1 on induced Tregs (iTregs) and their small extracellular vesicles (sEVs) by using a conditional knockout for Nrp1 on FoxP3+ cells. sEVs derived from iTregs were obtained by ultracentrifugation, purified using size exclusion columns, and characterized by nanoparticle tracking analysis. sEVs' impact on CD4+ T-cell cultures was evaluated using functional modulation assays, including CD4+ T-cell phenotypic analysis by flow cytometry and ELISA. We observed a decrease in iTreg induction when CD4+ T cells came from the Nrp1 knockout (KO) mice, indicating that Nrp1 is required for de novo FoxP3 induction/expression. Second, CD4+ T cells cultured with sEV-derived from wild-type (WT) iTregs reduced CD4+ T-cell proliferation, decreased the expression of CD25, and induced FoxP3 and CD73. In contrast, sEVs derived from Nrp1KO iTregs were unable to suppress CD4+ T-cell proliferation and to favor CD25 and CD73 expression. With respect to cytokine production, both sEVs derived from WT and Nrp1KO iTregs inhibited IL-10 and IFN-γ secretion, indicating that Nrp1 is not required for the regulation of these cytokines by sEV. Overall, this study provides new information into the role of Nrp1 in immunomodulation, revealing that Nrp1 signaling plays a role in iTreg differentiation by permitting FoxP3 expression and that iTreg-derived sEVs depend on Nrp1 to control CD4+ T-cell proliferation and phenotype.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13071156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147679108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bone marrow and splenic immune composition is unperturbed by short-term exposure to bedding from pet store mice. 骨髓和脾免疫组成不受短期暴露于宠物店小鼠床上用品的干扰。

ImmunoHorizons Pub Date : 2026-04-11 DOI: 10.1093/immhor/vlag014

Sarah E Little-Letsinger, Peer W F Karmaus, Michael B Fessler, Sara E Hamilton

{"title":"Bone marrow and splenic immune composition is unperturbed by short-term exposure to bedding from pet store mice.","authors":"Sarah E Little-Letsinger, Peer W F Karmaus, Michael B Fessler, Sara E Hamilton","doi":"10.1093/immhor/vlag014","DOIUrl":"10.1093/immhor/vlag014","url":null,"abstract":"Mice with natural microbial exposures (NMEs) have been proposed to be superior to specific pathogen-free (SPF) laboratory mice for modeling adult human immune and inflammatory profiles. Research using NME mice has focused on the effects of sustained exposure on peripheral blood and lymphoid and nonlymphoid organs. The effect of short-term NME is not known, in particular the impact to bone marrow immune composition. Male and female C57Bl/6J mice were exposed to SPF conditions for 6 wk (age 4 to 10 wk) with or without exposure to dirty bedding from pet store mice for the first week. At sacrifice, substantial shifts in the fecal bacteriome, at the phylum, order, and genus levels were evident in male and female NME mice, confirming induction of a new exposome with NME. However, only female NME mice had pathogens in their feces detectable by polymerase chain reaction (2 of 35). Numerous sex-dependent differences in T cell and myeloid composition in bone marrow and spleens were observed. We report several novel immune composition findings by sex, including higher proportions of Ki67+ regulatory and CD8+ T cells in female bone marrow. We detected 2 differences resulting from NME in the spleens of females, including increased PD-1 in CD44+CD8+ T cells and higher mean Foxp3 expression in regulatory T cells. We conclude that short-term exposure to pet store bedding is insufficient to induce robust changes in immune composition in spleens or bone marrow. Future research with the NME model should focus on sustained exposure and investigate exposure timing.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13071152/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147679682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cellular and molecular interactions underlying the peripheral immune responses to blood-stage malaria infections. 细胞和分子的相互作用是血液期疟疾感染的外周免疫反应的基础。

ImmunoHorizons Pub Date : 2026-04-11 DOI: 10.1093/immhor/vlag016

Kieran Tebben, Rosita Asawa, David Serre, Kirsten E Lyke

引用次数: 0

ZBP1 mediated restriction of Toxoplasma gondii in both the early acute and chronic brain stages of infection. ZBP1介导的弓形虫在早期急性和慢性脑感染阶段的限制。

ImmunoHorizons Pub Date : 2026-04-11 DOI: 10.1093/immhor/vlag015

Lydia Anne Sibley, Isaac William Babcock, Naa Dedee Amadi, Anne Elise Marchildon, Abigail Grace Kelly, Sydney Ann Labuzan, John Robert Lukens, Tajie Heartsong Harris

{"title":"ZBP1 mediated restriction of Toxoplasma gondii in both the early acute and chronic brain stages of infection.","authors":"Lydia Anne Sibley, Isaac William Babcock, Naa Dedee Amadi, Anne Elise Marchildon, Abigail Grace Kelly, Sydney Ann Labuzan, John Robert Lukens, Tajie Heartsong Harris","doi":"10.1093/immhor/vlag015","DOIUrl":"10.1093/immhor/vlag015","url":null,"abstract":"ZBP1 is an innate sensor of nucleic acids in the Z-conformation and regulates immune responses via cell death pathways and nuclear factor κB signaling. Previous work has demonstrated an essential role for ZBP1 in viral restriction; however, the role ZBP1 plays in protection against other pathogens is in early stages of exploration. Toxoplasma gondii is an obligate intracellular parasite that can infect all nucleated cells and establishes a chronic infection of the brain requiring a robust innate and adaptive immune response and multiple cell death pathways for host survival. Importantly, innate sensors of T. gondii infection of the central nervous system are still being defined. Prior work has implicated caspase-1 and caspase-8 in the control of T. gondii in the brain. Because ZBP1 can activate both caspase-1 and caspase-8, we sought to explore the role of ZBP1 during T. gondii infection. During early infection, we found an increase in parasite burden; a decrease in NK1.1+ cell, neutrophil, and monocyte recruitment; and impaired NK1.1+ cell cytokine production in the peritoneum of Zbp1-/- mice. Interestingly, during the early adaptive immune response, the immune cell recruitment defects and impaired parasite control were ameliorated. During the brain stage of infection, ZBP1 regulated parasite restriction and numerous inflammatory responses to infection. Our findings establish ZBP1 as a critical regulator of host defense to T. gondii and highlight the importance of ZBP1 in development of inflammation during both the acute and chronic infection.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13091654/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147719294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Temporal variability in healthy donor IFN-γ ELISpot responses reveals a stable IL-7-responsive functional metric for immune phenotyping. 健康供体IFN-γ ELISpot反应的时间变异性揭示了免疫表型的稳定il -7反应功能指标。

ImmunoHorizons Pub Date : 2026-04-11 DOI: 10.1093/immhor/vlag021

Annemarie Nguyen, Ruth-Ann Brown, Anthony S Bonavia

引用次数: 0

Presentation of the protective epitope in a Chlamydia muridarum MOMP vaccine is dependent on γ-interferon-inducible lysosomal thiol reductase (GILT). muridarum衣原体MOMP疫苗中保护性表位的呈现依赖于γ-干扰素诱导溶酶体硫醇还原酶（GILT）。

ImmunoHorizons Pub Date : 2026-04-11 DOI: 10.1093/immhor/vlag018

Sukumar Pal, Raymond M Johnson, Delia F Tifrea, Peter Cresswell, Luis M de la Maza

{"title":"Presentation of the protective epitope in a Chlamydia muridarum MOMP vaccine is dependent on γ-interferon-inducible lysosomal thiol reductase (GILT).","authors":"Sukumar Pal, Raymond M Johnson, Delia F Tifrea, Peter Cresswell, Luis M de la Maza","doi":"10.1093/immhor/vlag018","DOIUrl":"10.1093/immhor/vlag018","url":null,"abstract":"The Chlamydia outer membrane complex has approximately 20 cysteine-rich proteins, including the major outer membrane protein (MOMP) with 8 cysteines. The enzyme γ-interferon-inducible lysosomal thiol reductase (GILT) is expressed constitutively in lysosomes of antigen presenting cells and reproductive tract epithelial cells. GILT catalyzes disulfide bond reduction during protein degradation that generates T cell epitopes. To evaluate the role that GILT plays in chlamydial infections, C57BL/6 WT mice and mice deficient in Ifi30 (GILT-KO) were challenged vaginally with Chlamydia muridarum (Cm). Both were equally susceptible to the Cm infection and upper genital tract pathology. To assess GILT's role in processing MOMP epitopes, WT and GILT-KO mice were immunized with native (nMOMP) or recombinant (rMOMP) antigens. In both strains vaccination with Cm nMOMP and rMOMP induced a similar spectrum of MOMP-specific antibodies. nMOMP immunization generated higher neutralizing antibody titers than rMOMP, but neutralizing titers did not differ between mouse strains. Splenocytes from vaccinated WT and GILT-KO mice recognized T cell epitopes in nMOMP, and to a lesser extent with rMOMP. No protection was seen in either WT or GILT-KO mice vaccinated with rMOMP based on intensity and duration of vaginal shedding, upper genital tract pathology, and fertility post-infection. nMOMP vaccination protected WT mice based on attenuated bacterial shedding and preserved fertility but nMOMP-vaccinated GILT-KO mice were not protected. The failure of nMOMP vaccination in GILT-KO mice revealed that GILT-dependent MOMP epitope processing was outcome determinative and identified a pan-serovar, likely protective, class II T cell epitope in MOMP constant domain 3.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13082905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147694245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clonal amplification of peripheral CD4+ and CD8+ T cells is associated with clinical response to checkpoint blockade in chronic hepatitis B. 慢性乙型肝炎患者外周血CD4+和CD8+ T细胞克隆扩增与检查点阻断的临床反应相关。

ImmunoHorizons Pub Date : 2026-04-11 DOI: 10.1093/immhor/vlag020

Samuel C Kim, Christopher Richards, Mario Cortese, Julie J Lin, Jeffrey J Wallin

{"title":"Clonal amplification of peripheral CD4+ and CD8+ T cells is associated with clinical response to checkpoint blockade in chronic hepatitis B.","authors":"Samuel C Kim, Christopher Richards, Mario Cortese, Julie J Lin, Jeffrey J Wallin","doi":"10.1093/immhor/vlag020","DOIUrl":"10.1093/immhor/vlag020","url":null,"abstract":"Therapeutic strategies for chronic hepatitis B (CHB) aim to achieve functional cure, specifically defined by sustained off-treatment elimination of hepatitis B virus (HBV) surface antigen. New treatment approaches are being developed to enhance HBV-specific immune responses to reach this goal. To better understand how checkpoint blockade works in CHB, we conducted single-cell sequencing analysis of blood samples from four patients who either responded or did not respond to a single dose of nivolumab (an anti-PD-1 therapy). We examined cells at baseline and at two subsequent timepoints during treatment. Our findings revealed that a patient who achieved functional cure displayed higher baseline levels of stem cell-like memory CD8+ T cells, along with increases in CD8+ T effector cells, CD8+ T effector memory cells, and CD4+ T cells that reexpress CD45RA at 24 weeks after nivolumab administration. Additionally, we observed the emergence of specific T and B cell clones during treatment that correlated with positive response. These clones were identified within CD8 T effector, CD8 T effector memory, CD4 T memory cells re-expressing CD45RA, and memory B cell populations. Notably, some prominent memory B cell clones had not undergone isotype switching, indicating the development of new B cell responses rather than modification of existing immune responses. These results suggest that certain T cell phenotypes in peripheral blood, together with specific clonal expansions of T and B cells, may indicate successful clinical response to checkpoint blockade therapy in CHB. Developing treatments that specifically enhance these immune mechanisms may lead to more effective therapeutic strategies.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Direct contact with natural killer cells reprograms monocyte-derived dendritic cells into a tolerogenic phenotype. 与自然杀伤细胞的直接接触将单核细胞衍生的树突状细胞重新编程为耐受性表型。

ImmunoHorizons Pub Date : 2026-03-10 DOI: 10.1093/immhor/vlag007

Ammar J Alsheikh, Liang Chen, Daniel Korenfeld, Jason Tam, Suresh Patil, Hsi-Ju Wei, Jianing Li, Suju Zhong, Feng Dong, Terry Melim, Karin Orsi, Samuel Karsen, Yingli Yang, Susan Westmoreland, Aridaman Pandit, Kevin White, Timothy Radstake, Abel Suarez-Fueyo

{"title":"Direct contact with natural killer cells reprograms monocyte-derived dendritic cells into a tolerogenic phenotype.","authors":"Ammar J Alsheikh, Liang Chen, Daniel Korenfeld, Jason Tam, Suresh Patil, Hsi-Ju Wei, Jianing Li, Suju Zhong, Feng Dong, Terry Melim, Karin Orsi, Samuel Karsen, Yingli Yang, Susan Westmoreland, Aridaman Pandit, Kevin White, Timothy Radstake, Abel Suarez-Fueyo","doi":"10.1093/immhor/vlag007","DOIUrl":"10.1093/immhor/vlag007","url":null,"abstract":"Tissue-infiltrating monocyte-derived dendritic cells (DCs) and macrophages are key antigen-presenting cells promoting inflammation and tissue damage by releasing proinflammatory cytokines and strongly activating T cells. These antigen-presenting cells are prominent in inflamed tissues, including in conditions such as inflammatory bowel disease. Modulating the number or function of these cells presents an opportunity to mitigate inflammation and promote immune tolerance in inflammatory disorders. In this study, we comprehensively evaluate a novel approach to modulate these cell populations. First, we employ an antibody-mediated approach to selectively deplete inflammatory DCs while simultaneously reprogramming surviving cells toward a tolerogenic phenotype. Second, we utilize a natural killer-DC co-culture system to dissect molecular mechanisms of DC tolerance induction through integrated transcriptomic and epigenomic analysis, complemented by functional assays. We confirm that the generated DCs exhibit tolerogenic properties, marked by a reduced ability to induce allogenic T-cell activation, increased expression of regulatory mediators including IL-10 and IDO1, and decreased levels of co-stimulatory and activation markers such as CD11c, CD40, and CD44. Finally, using CRISPR knockout, we confirm the essential role of transcription factors IKZF1 and PU.1 in this process. Our findings advance the understanding of how epigenetic remodeling and transcription factor activity govern DC tolerance, and highlight promising therapeutic avenues for DC-targeted therapeutic approaches in inflammatory disorders.","PeriodicalId":94037,"journal":{"name":"ImmunoHorizons","volume":"10 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13020354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0