Yahui Guo,Mariano A Aufiero,Kathleen Am Mills,Simon A Grassmann,Hyunu Kim,Mergim Gjonbalaj,Paul Zumbo,Audrey Billips,Katrina B Mar,Yao Yu,Laura Echeverri Tirado,Lena Heung,Amariliz Rivera,Doron Betel,Joseph C Sun,Tobias M Hohl
{"title":"An IFN/STAT1/CYBB Axis Defines Protective Plasmacytoid DC to Neutrophil Crosstalk in Aspergillus fumigatus - Infected mice.","authors":"Yahui Guo,Mariano A Aufiero,Kathleen Am Mills,Simon A Grassmann,Hyunu Kim,Mergim Gjonbalaj,Paul Zumbo,Audrey Billips,Katrina B Mar,Yao Yu,Laura Echeverri Tirado,Lena Heung,Amariliz Rivera,Doron Betel,Joseph C Sun,Tobias M Hohl","doi":"10.1172/jci190107","DOIUrl":"https://doi.org/10.1172/jci190107","url":null,"abstract":"Aspergillus fumigatus is the most common cause of invasive aspergillosis (IA), a devastating infection in immunocompromised patients. Plasmacytoid dendritic cells (pDCs) regulate host defense against IA by enhancing neutrophil antifungal properties in the lung. Here, we define the pDC activation trajectory during A. fumigatus infection and the molecular events that underlie the protective pDC - neutrophil crosstalk. Fungus-induced pDC activation begins after bone marrow egress and results in pDC-dependent regulation of lung type I and type III IFN levels. These pDC-derived products act on type I and type III IFN receptor-expressing neutrophils and control neutrophil fungicidal activity and reactive oxygen species production via STAT1 signaling in a cell-intrinsic manner. Mechanistically, neutrophil STAT1 signaling regulates the transcription and expression of Cybb, which encodes one of five NADPH oxidase subunits. Thus, pDCs regulate neutrophil-dependent immunity against inhaled molds by controlling the local expression of a subunit required for NADPH oxidase assembly and activity in the lung.","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144787434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tao Zhen,Yaqiang Cao,Tongyi Dou,Yun Chen,Guadalupe Lopez,Ana Catarina Menezes,Xufeng Wu,John Hammer,Jun Cheng,Lisa Garrett,Stacie Anderson,Martha Kirby,Stephen Wincovitch,Bayu Sisay,Abdel G Elkahloun,Di Wu,Lucio H Castilla,Wei Yang,Jiansen Jiang,Keji Zhao,Paul P Liu
{"title":"CBFβ-SMMHC-driven leukemogenesis requires enhanced RUNX1-DNA binding affinity in mice.","authors":"Tao Zhen,Yaqiang Cao,Tongyi Dou,Yun Chen,Guadalupe Lopez,Ana Catarina Menezes,Xufeng Wu,John Hammer,Jun Cheng,Lisa Garrett,Stacie Anderson,Martha Kirby,Stephen Wincovitch,Bayu Sisay,Abdel G Elkahloun,Di Wu,Lucio H Castilla,Wei Yang,Jiansen Jiang,Keji Zhao,Paul P Liu","doi":"10.1172/jci192923","DOIUrl":"https://doi.org/10.1172/jci192923","url":null,"abstract":"The leukemia fusion gene CBFB-MYH11 requires RUNX1 for leukemogenesis, but the underlying mechanism is unclear. By in vitro studies, we found that CBFβ-SMMHC, the chimeric protein encoded by CBFB-MYH11, could enhance the binding affinity between RUNX1 and its target DNA. Increased RUNX1-DNA binding was also observed in myeloid progenitor cells from mice expressing CBFβ-SMMHC. Moreover, only CBFβ-SMMHC variants able to enhance the DNA binding affinity by RUNX1 could induce leukemia in mouse models. Marked transcriptomic changes, affecting genes associated with inflammatory response and target genes of CBFA2T3, were observed in mice expressing leukemogenic CBFβ-SMMHC variants. Finally, we show that CBFβ-SMMHC could not induce leukemia in mice with a Runx1-R188Q mutation, which reduces RUNX1 DNA binding but not affecting its interaction with CBFβ-SMMHC or its sequestration to cytoplasm by CBFβ-SMMHC. Our data suggest that, in addition to binding RUNX1 to regulate gene expression, enhancing RUNX1 binding affinity to its target DNA is an important mechanism by which CBFβ-SMMHC contributes to leukemogenesis, highlighting RUNX1-DNA interaction as a potential therapeutic target in inv(16) AML.","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144787155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Jab1 promotes immune evasion and progression in acute myeloid leukemia models under oxidative stress.","authors":"Nan Zhang,Qian Wang,Guopeng Chen,Li Liu,Zhiying Wang,Linlu Ma,Yuxing Liang,Jinxian Wu,Xinqi Li,Xiaoyan Liu,Fuling Zhou","doi":"10.1172/jci183761","DOIUrl":"https://doi.org/10.1172/jci183761","url":null,"abstract":"Acute myeloid leukemia (AML) is the most common hematological malignancy. Leukemia stem cells exhibit high levels of oxidative stress, with reactive oxygen species (ROS) being the primary products of this stress, inducing the expression of Jab1. Previous studies have demonstrated that Jab1, as a transcriptional coactivator of c-JUN, promotes the malignant progression of AML under oxidative stress. However, its role in immune evasion is still under investigation. Here, we observed that knocking out Jab1 reduced the expression of immune checkpoints in vivo, effectively overcame the immune evasion of AML. Interestingly, the deletion of Jab1 had no impact on the maturation of normal hematopoietic cells in mice. Mechanistically, Jab1 directly activated IGF2BP3 by driving the transcription factor c-JUN, consequently modulated the m6A modification of LILRB4 mRNA and promoted immune evasion in AML. Finally, CSN5i-3 effectively disrupted the signaling pathway mediated by Jab1, thereby restoring cellular immune surveillance and halting the progression of AML. Thus, our results highlight the functional role of Jab1 in supporting AML survival and support the development of targeted therapeutic strategies.","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"161 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144787156","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Himanshu Savardekar,Andrew Stiff,Alvin Liu,Robert Wesolowski,Emily Schwarz,Ian C Garbarine,Megan C Duggan,Sara Zelinskas,Jianying Li,Gabriella Lapurga,Alexander Abreo,Lohith Savardekar,Ryan Parker,Julia Sabella,Mallory J DiVincenzo,Brooke Benner,Steven H Sun,Dionisia Quiroga,Luke Scarberry,Gang Xin,Anup Dey,Keiko Ozato,Lianbo Yu,Merve Hasanov,Debasish Sundi,Richard C Wu,Kari L Kendra,William E Carson Iii
{"title":"BRD4 inhibition leads to MDSC apoptosis and enhances checkpoint blockade therapy.","authors":"Himanshu Savardekar,Andrew Stiff,Alvin Liu,Robert Wesolowski,Emily Schwarz,Ian C Garbarine,Megan C Duggan,Sara Zelinskas,Jianying Li,Gabriella Lapurga,Alexander Abreo,Lohith Savardekar,Ryan Parker,Julia Sabella,Mallory J DiVincenzo,Brooke Benner,Steven H Sun,Dionisia Quiroga,Luke Scarberry,Gang Xin,Anup Dey,Keiko Ozato,Lianbo Yu,Merve Hasanov,Debasish Sundi,Richard C Wu,Kari L Kendra,William E Carson Iii","doi":"10.1172/jci181975","DOIUrl":"https://doi.org/10.1172/jci181975","url":null,"abstract":"BRD4 is an epigenetic reader protein that regulates oncogenes such as myc in cancer. However, its additional role in shaping immune responses via regulation of inflammatory and myeloid cell responses is not yet fully understood. This work further characterized the multifaceted role of BRD4 in anti-tumor immunity. NanoString gene expression analysis of EMT6 tumors treated with a BRD4 inhibitor identified a reduction in myeloid gene expression signatures. Additionally, BRD4 inhibition significantly reduced myeloid derived suppressor cells (MDSC) in the spleens and tumors of mice in multiple tumor models and also decreased the release of tumor-derived MDSC growth and chemotactic factors. Pharmacologic inhibition of BRD4 in MDSC induced apoptosis and modulated expression of apoptosis regulatory proteins. A BRD4-myeloid specific knockout model suggested that the dominant mechanism of MDSC reduction after BRD4 inhibition was primarily through a direct effect on MDSC. BRD4 inhibition enhanced anti-PD-L1 therapy in the EMT6, 4T1, and LLC tumor models, and the efficacy of the combination treatment was dependent on CD8+ T cells and on BRD4 expression in the myeloid compartment. These results identify BRD4 as a regulator of MDSC survival and provide evidence to further investigate BRD4 inhibitors in combination with immune based therapies.","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"16 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144787158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alyssa M Duffy,Anshika Goenka,Maryam I Azeem,Azmain Taz,Sayalee V Potdar,Sara A Scott,Ellen Marin,Jonathan L Kaufman,Craig C Hofmeister,Nisha S Joseph,Vikas A Gupta,Sagar Lonial,Ajay K Nooka,Madhav V Dhodapkar,Kavita M Dhodapkar
{"title":"Early CD4+ T-cell proliferative burst and chronic T-cell engagement impact myeloma outcomes following T-cell engager therapy.","authors":"Alyssa M Duffy,Anshika Goenka,Maryam I Azeem,Azmain Taz,Sayalee V Potdar,Sara A Scott,Ellen Marin,Jonathan L Kaufman,Craig C Hofmeister,Nisha S Joseph,Vikas A Gupta,Sagar Lonial,Ajay K Nooka,Madhav V Dhodapkar,Kavita M Dhodapkar","doi":"10.1172/jci192927","DOIUrl":"https://doi.org/10.1172/jci192927","url":null,"abstract":"","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144778163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Matthew Wortham,Bastian Ramms,Chun Zeng,Jacqueline R Benthuysen,Somesh Sai,Dennis P Pollow,Fenfen Liu,Michael Schlichting,Austin R Harrington,Bradley Liu,Thazha P Prakash,Elaine C Pirie,Han Zhu,Siyouneh Baghdasarian,Sean T Lee,Victor A Ruthig,Kristen L Wells,Johan Auwerx,Orian S Shirihai,Maike Sander
{"title":"The protein deacetylase SIRT2 exerts metabolic control over adaptive β cell proliferation.","authors":"Matthew Wortham,Bastian Ramms,Chun Zeng,Jacqueline R Benthuysen,Somesh Sai,Dennis P Pollow,Fenfen Liu,Michael Schlichting,Austin R Harrington,Bradley Liu,Thazha P Prakash,Elaine C Pirie,Han Zhu,Siyouneh Baghdasarian,Sean T Lee,Victor A Ruthig,Kristen L Wells,Johan Auwerx,Orian S Shirihai,Maike Sander","doi":"10.1172/jci187020","DOIUrl":"https://doi.org/10.1172/jci187020","url":null,"abstract":"Selective and controlled expansion of endogenous β-cells has been pursued as a potential therapy for diabetes. Ideally, such therapies would preserve feedback control of β-cell proliferation to avoid excessive β-cell expansion. Here, we identified a regulator of β-cell proliferation whose inactivation results in controlled β-cell expansion: the protein deacetylase Sirtuin 2 (SIRT2). Sirt2 deletion in β-cells of mice increased β-cell proliferation during hyperglycemia with little effect in homeostatic conditions, indicating preservation of feedback control of β-cell mass. SIRT2 restrains proliferation of human islet β-cells, demonstrating conserved SIRT2 function. Analysis of acetylated proteins in islets treated with a SIRT2 inhibitor revealed that SIRT2 deacetylates enzymes involved in oxidative phosphorylation, dampening the adaptive increase in oxygen consumption during hyperglycemia. At the transcriptomic level, Sirt2 inactivation has context-dependent effects on β-cells, with Sirt2 controlling how β-cells interpret hyperglycemia as a stress. Finally, we provide proof-of-principle that systemic administration of a GLP1-coupled Sirt2-targeting antisense oligonucleotide achieves β-cell Sirt2 inactivation and stimulates β-cell proliferation during hyperglycemia. Overall, these studies identify a therapeutic strategy for increasing β-cell mass in diabetes without circumventing feedback control of β-cell proliferation. Future work should test the extent that these findings translate to human β-cells from individuals with and without diabetes.","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144778187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Michelle W Cheung,Samantha Xu,Janna R Shapiro,Freda Qi,Melanie Delgado-Brand,Karen Colwill,Roya Dayam,Ying Liu,Jenny Choi,Joanne M Stempak,James M Rini,Vinod Chandran,Mark S Silverberg,Anne-Claude Gingras,Tania H Watts
{"title":"Reduced vaccine-induced germinal center outputs in inflammatory bowel disease patients treated with anti-TNF biologics.","authors":"Michelle W Cheung,Samantha Xu,Janna R Shapiro,Freda Qi,Melanie Delgado-Brand,Karen Colwill,Roya Dayam,Ying Liu,Jenny Choi,Joanne M Stempak,James M Rini,Vinod Chandran,Mark S Silverberg,Anne-Claude Gingras,Tania H Watts","doi":"10.1172/jci192589","DOIUrl":"https://doi.org/10.1172/jci192589","url":null,"abstract":"BACKGROUNDAnti-TNF biologics are widely used to treat patients with immune-mediated inflammatory diseases. In mouse models, the complete absence of TNF impairs germinal center (GC) responses. Less is known about the impact of anti-TNF therapy on specific immune responses in humans. Widespread vaccination against SARS-CoV-2 offered an unprecedented opportunity to investigate the effects of biological therapies on responses to specific immunization. Previous work demonstrated that inflammatory bowel disease (IBD) patients treated with anti-TNF biologics exhibit decreased Spike-specific antibody responses compared to IBD patients treated with anti-IL-12/23 or healthy controls, even after four doses of mRNA vaccine.METHODSHere we analyzed humoral responses to SARS-CoV-2 immunization using single-cell RNA-Sequencing and flow cytometry of Spike-specific memory B cells (MBC), as well as avidity measurements of plasma antibodies from IBD patients treated with anti-TNF or anti-IL-12/23 or from healthy controls.RESULTSWe observed decreased somatic hypermutation in the B cell receptors of Spike-specific MBCs and decreased antigen-specific MBC accumulation following SARS-CoV-2 mRNA vaccination in anti-TNF treated IBD patients, compared to IBD patients treated with anti-IL-12/23 or healthy controls. This decreased somatic hypermutation in Spike-specific MBCs in anti-TNF treated patients correlated with decreased and delayed antibody affinity maturation and reduced neutralization activity.CONCLUSIONThese data provide in vivo evidence that anti-TNF, but not anti-IL-12/23, therapy impairs the quantity and quality of antigen-specific GC outputs in humans.FUNDINGJuan and Stefania Speck (donation) and by Canadian Institutes of Health Research (CIHR)/COVID-Immunity Task Force (CITF) grants VR-1 172711, VS1-175545, GA2-177716, GA1-177703 and CIHR FDN 143301 &143350.","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"15 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sahitya Saka,Zhanping Lu,Yinghua Wang,Peng Liu,Deependra K Singh,Junki P Lee,Carmen G Palii,Tyler R Alvarez,Anna L F V Assumpção,Xiaona You,Jing Zhang,Marjorie Brand,Michael L Atchison,Xuan Pan
{"title":"Chromatin factor YY1 controls fetal hematopoietic stem cell migration and engraftment in mice.","authors":"Sahitya Saka,Zhanping Lu,Yinghua Wang,Peng Liu,Deependra K Singh,Junki P Lee,Carmen G Palii,Tyler R Alvarez,Anna L F V Assumpção,Xiaona You,Jing Zhang,Marjorie Brand,Michael L Atchison,Xuan Pan","doi":"10.1172/jci188140","DOIUrl":"https://doi.org/10.1172/jci188140","url":null,"abstract":"The fetal liver is the primary site of hematopoietic stem cell (HSC) generation during embryonic development. However, the molecular mechanisms governing the transition of hematopoiesis from the fetal liver to the bone marrow (BM) remain incompletely understood. Here, we identify the mammalian Polycomb group (PcG) protein Yin Yang 1 (YY1) as a key regulator of this developmental transition. Conditional deletion of Yy1 in the hematopoietic system during fetal development results in neonatal lethality and depletion of the fetal HSC pool. YY1-deficient fetal HSCs exhibit impaired migration and fail to engraft in the adult BM, thereby losing their ability to reconstitute hematopoiesis. Transcriptomic analysis reveals that Yy1 knockout disrupts genetic networks controlling cell motility and adhesion in fetal hematopoietic stem and progenitor cells (HSPCs). Notably, YY1 does not directly bind the promoters of most dysregulated genes. Instead, it modulates chromatin accessibility at regulatory loci, orchestrating broader epigenetic programs essential for HSPC migration and adhesion. Together, these findings establish YY1 as a critical epigenetic regulator of fetal HSC function and provide a mechanistic framework to further decipher how temporal epigenomic configurations determine HSC fetal-to-adult transition during development.","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"87 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144778164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Natalie F McMyn,Joseph Varriale,Hanna W S Wu,Vivek Hariharan,Milica Moskovljevic,Toong Seng Tan,Jun Lai,Anushka Singhal,Kenneth Lynn,Karam Mounzer,Pablo Tebas,Luis J Montaner,Rebecca Hoh,Xu G Yu,Mathias Lichterfeld,Francesco R Simonetti,Colin Kovacs,Steven G Deeks,Janet M Siliciano,Robert F Siliciano
{"title":"Factors associated with resistance of HIV-1 reservoir viruses to neutralization by autologous IgG antibodies.","authors":"Natalie F McMyn,Joseph Varriale,Hanna W S Wu,Vivek Hariharan,Milica Moskovljevic,Toong Seng Tan,Jun Lai,Anushka Singhal,Kenneth Lynn,Karam Mounzer,Pablo Tebas,Luis J Montaner,Rebecca Hoh,Xu G Yu,Mathias Lichterfeld,Francesco R Simonetti,Colin Kovacs,Steven G Deeks,Janet M Siliciano,Robert F Siliciano","doi":"10.1172/jci194081","DOIUrl":"https://doi.org/10.1172/jci194081","url":null,"abstract":"Antiretroviral therapy (ART) prevents HIV-1 replication but does not eliminate the latent reservoir, the source of viral rebound if treatment is stopped. Autologous neutralizing antibodies (aNAbs) can block in vitro outgrowth of a subset of reservoir viruses and therefore potentially affect viral rebound upon ART interruption. We investigated aNAbs in 31 people with HIV-1 (PWH) on ART. Participants fell into two groups based on a high or low fraction of aNAb-resistant reservoir isolates, with most isolates being aNAb-resistant (IC50 >100 μg/ml). Time on uninterrupted ART was associated with higher aNAb resistance. However, pharmacodynamic analysis predicted that many isolates would be partially inhibited at physiologic IgG concentrations, to the same degree as by single antiretroviral drugs. Steep dose-response curve slopes, an indication of cooperativity, were observed for the rare isolates that were very strongly inhibited (>5 logs) by aNAbs. Resistance to aNAbs was not fully explained by declining in aNAb titers and may be driven partially by ADCC-mediated elimination of infected cells carrying aNAb-sensitive viruses over long time intervals, leaving only aNAb-resistant viruses which can contribute to viral rebound.","PeriodicalId":520097,"journal":{"name":"The Journal of Clinical Investigation","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144737392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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