Andrew W Simonson, Joseph J Zeppa, Allison N Bucsan, Michael C Chao, Supriya Pokkali, Forrest Hopkins, Michael R Chase, Andrew J Vickers, Matthew S Sutton, Caylin G Winchell, Amy J Myers, Cassaundra L Ameel, Ryan J Kelly, Ben Krouse, Luke E Hood, Jiaxiang Li, Chelsea C Lehman, Megha Kamath, Jaime Tomko, Mark A Rodgers, Rachel Donlan, Harris Chishti, H Jacob Borish, Edwin Klein, Charles A Scanga, Sarah M Fortune, Philana Ling Lin, Pauline Maiello, Mario Roederer, Patricia A Darrah, Robert A Seder, JoAnne L Flynn
{"title":"Intravenous BCG-mediated protection against tuberculosis requires CD4+ T cells and CD8α+ lymphocytes.","authors":"Andrew W Simonson, Joseph J Zeppa, Allison N Bucsan, Michael C Chao, Supriya Pokkali, Forrest Hopkins, Michael R Chase, Andrew J Vickers, Matthew S Sutton, Caylin G Winchell, Amy J Myers, Cassaundra L Ameel, Ryan J Kelly, Ben Krouse, Luke E Hood, Jiaxiang Li, Chelsea C Lehman, Megha Kamath, Jaime Tomko, Mark A Rodgers, Rachel Donlan, Harris Chishti, H Jacob Borish, Edwin Klein, Charles A Scanga, Sarah M Fortune, Philana Ling Lin, Pauline Maiello, Mario Roederer, Patricia A Darrah, Robert A Seder, JoAnne L Flynn","doi":"10.1084/jem.20241571","DOIUrl":"10.1084/jem.20241571","url":null,"abstract":"<p><p>Tuberculosis (TB) is a major health burden worldwide despite widespread intradermal (ID) BCG vaccination in newborns. We previously demonstrated that changing the BCG route and dose from 5 × 105 CFUs ID to 5 × 107 CFUs i.v. resulted in prevention of Mycobacterium tuberculosis (Mtb) infection and TB disease in highly susceptible nonhuman primates. Identifying immune mechanisms protection following i.v. BCG will facilitate development of more effective vaccines against TB. Here, we depleted lymphocyte subsets prior to and during Mtb challenge in i.v. BCG-vaccinated macaques to identify those necessary for protection. Depletion of adaptive CD4 T cells, but not adaptive CD8αβ T cells, resulted in loss of protection with increased Mtb burdens and dissemination, indicating that CD4 T cells are critical to i.v. BCG-mediated protection. Depletion of unconventional CD8α-expressing lymphocytes (NK cells, innate T cells, and CD4+CD8α+ double-positive T cells) abrogated protection in most i.v. BCG-immunized macaques, supporting further investigation into which of these cell subsets contribute to protection after vaccination.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 4","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11801270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143255794","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}
Zhe Chen, Feng Wu, Yan Li, Lei Li, Yufei Lei, Siwei Gao, Tao Chen, Yuxin Xie, Jianwen Xiao, Hanqing Zeng, Jianchuan Deng, Xueya Zhao, Yu Hou
{"title":"Inhibition of DEK restores hematopoietic stem cell function in Fanconi anemia.","authors":"Zhe Chen, Feng Wu, Yan Li, Lei Li, Yufei Lei, Siwei Gao, Tao Chen, Yuxin Xie, Jianwen Xiao, Hanqing Zeng, Jianchuan Deng, Xueya Zhao, Yu Hou","doi":"10.1084/jem.20241248","DOIUrl":"https://doi.org/10.1084/jem.20241248","url":null,"abstract":"<p><p>Hematopoietic stem cells (HSCs) are susceptible to replication stress, which is a major contributor to HSC defects in Fanconi anemia (FA). Here, we report that HSCs relax the global chromatin by downregulating the expression of a chromatin architectural protein, DEK, in response to replication stress. DEK is abnormally accumulated in bone marrow (BM) CD34+ cells from patients with FA and in Fancd2-deficient HSCs. DEK haploinsufficiency promotes chromatin relaxation, replication stress relief, and function recovery of Fancd2-deficient HSCs. Furthermore, inhibition of DEK restores the proliferation of FA CD34+ cells in vitro and enhances their engraftment in vivo. Mechanistically, the activating transcription factor 2 (ATF2), specifically phosphorylated ATF2 at Thr69/71, was identified as a promoter of DEK transcription. Fancd2 deficiency results in p38 hyperphosphorylation, which in turn phosphorylates ATF2 at Thr69/71, leading to DEK accumulation in HSCs. In conclusion, our findings establish a functional link between chromatin relaxation and replication stress tolerance in HSCs and highlight DEK as a target for FA.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11748990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059203","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}
Shan Miao, Hao Li, Xiaohan Song, Yongbo Liu, Gaoyang Wang, Chen Kan, Youqiong Ye, Ru-Juan Liu, Hua-Bing Li
{"title":"tRNA m1A modification regulates cholesterol biosynthesis to promote antitumor immunity of CD8+ T cells.","authors":"Shan Miao, Hao Li, Xiaohan Song, Yongbo Liu, Gaoyang Wang, Chen Kan, Youqiong Ye, Ru-Juan Liu, Hua-Bing Li","doi":"10.1084/jem.20240559","DOIUrl":"10.1084/jem.20240559","url":null,"abstract":"<p><p>Activation of CD8+ T cells necessitates rapid metabolic reprogramming to fulfill the substantial biosynthetic demands of effector functions. However, the posttranscriptional mechanisms underpinning this process remain obscure. The transfer RNA (tRNA) N1-methyladenine (m1A) modification, essential for tRNA stability and protein translation, has an undefined physiological function in CD8+ T cells, particularly in antitumor responses. Here, we demonstrate that the tRNA m1A \"writer\" gene Trmt61a enhances the tumor-killing capacity of CD8+ T cells by regulating cholesterol biosynthesis. Deletion of Trmt61a in CD8+ T cells leads to a compromised tumor-killing function in both in vivo and in vitro assays. Mechanistically, tRNA m1A promotes antitumor immunity in CD8+ T cells by enhancing the translation of ATP citrate lyase, a key enzyme for cholesterol biosynthesis. Cholesterol supplementation rescues the impaired tumor-killing function and proliferation of TRMT61A-deficient CD8+ T cells. Our findings highlight tRNA m1A modification as a regulatory checkpoint in cholesterol metabolism in CD8+ T cells, suggesting potential novel strategies for cancer immunotherapy.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059297","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}
Yong Du, Bérénice Faz-Lopez, Marie Dominique Ah Kioon, Claire Cenac, Michael Pierides, Kimberly S Lakin, Robert F Spiera, Julie Chaumeil, Marie-Elise Truchetet, Jessica K Gordon, Jean-Charles Guéry, Franck J Barrat
{"title":"Altered X-chromosome inactivation of the TLR7/8 locus and heterogeneity of pDCs in systemic sclerosis.","authors":"Yong Du, Bérénice Faz-Lopez, Marie Dominique Ah Kioon, Claire Cenac, Michael Pierides, Kimberly S Lakin, Robert F Spiera, Julie Chaumeil, Marie-Elise Truchetet, Jessica K Gordon, Jean-Charles Guéry, Franck J Barrat","doi":"10.1084/jem.20231809","DOIUrl":"10.1084/jem.20231809","url":null,"abstract":"<p><p>Systemic sclerosis (SSc) is an autoimmune disease that has a strong female predominance. Both the X-linked TLR7 and TLR8 can induce type I IFN (IFN-I) by plasmacytoid DCs (pDCs), which can promote fibrosis. We identified five subclusters of pDCs, including ISGhigh clusters that were over-represented in SSc patients. We observed that both TLR7 and TLR8 genes escape from X chromosome inactivation (XCI) at higher frequency in pDCs of SSc patients, which was associated with changes in TLR7 protein profile. Combined DNA/RNA FISH analysis revealed that the TLR7/8 locus is preferentially located outside of the inactive X (Xi) territory when TLR7 is expressed, suggesting that higher-order loop formation is linked to TLR7/8 expression from the Xi. Furthermore, the expression levels of XIST and the transcriptional repressor SPEN were reduced in SSc pDCs. Hence, our data revealed the heterogeneity of pDCs in SSc and suggested that altered XCI at the TLR7/8 locus may contribute to the chronic IFN-I activity of pDCs in female SSc patients.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11639950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818248","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}
Carlos Gomez-Diaz, Wilhelm Greulich, Benedikt Wefers, Meiyue Wang, Silvia Bolsega, Maike Effern, Daniel P Varga, Zhe Han, Minyi Chen, Marleen Bérouti, Natascia Leonardi, Ulrike Schillinger, Bernhard Holzmann, Arthur Liesz, Axel Roers, Michael Hölzel, Marijana Basic, Wolfgang Wurst, Veit Hornung
{"title":"RNase T2 restricts TLR13-mediated autoinflammation in vivo.","authors":"Carlos Gomez-Diaz, Wilhelm Greulich, Benedikt Wefers, Meiyue Wang, Silvia Bolsega, Maike Effern, Daniel P Varga, Zhe Han, Minyi Chen, Marleen Bérouti, Natascia Leonardi, Ulrike Schillinger, Bernhard Holzmann, Arthur Liesz, Axel Roers, Michael Hölzel, Marijana Basic, Wolfgang Wurst, Veit Hornung","doi":"10.1084/jem.20241424","DOIUrl":"10.1084/jem.20241424","url":null,"abstract":"<p><p>RNA-sensing TLRs are strategically positioned in the endolysosome to detect incoming nonself RNA. RNase T2 plays a critical role in processing long, structured RNA into short oligoribonucleotides that engage TLR7 or TLR8. In addition to its positive regulatory role, RNase T2 also restricts RNA recognition through unknown mechanisms, as patients deficient in RNase T2 suffer from neuroinflammation. Consistent with this, mice lacking RNase T2 exhibit interferon-dependent neuroinflammation, impaired hematopoiesis, and splenomegaly. However, the mechanism by which RNase T2 deficiency unleashes inflammation in vivo remains unknown. Here, we report that the inflammatory phenotype found in Rnaset2-/- mice is completely reversed in the absence of TLR13, suggesting aberrant accumulation of an RNA ligand for this receptor. Interestingly, this TLR13-driven inflammatory phenotype is also fully present in germ-free mice, suggesting a role for RNase T2 in limiting erroneous TLR13 activation by an as yet unidentified endogenous ligand. These results establish TLR13 as a potential self-sensor that is kept in check by RNase T2.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032941","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}
{"title":"Kazuyo Moro: Building relationships is essential for gaining both speed and opportunities in research.","authors":"Montserrat Cols","doi":"10.1084/jem.20242176","DOIUrl":"10.1084/jem.20242176","url":null,"abstract":"<p><p>Professor Kazuyo Moro holds dual appointments as a team leader for the Laboratory for Innate Immune Systems at RIKEN IMS as well as Osaka University Graduate School of Medicine. Her lab conducts multifaceted research on type 2 innate lymphoid cells (ILC2), from ILC2 differentiation, activation, suppression, and transcriptional control mechanisms, as well as basic research and drug discovery. The research from Prof. Moro lab aims to build new models and therapies for related immune diseases such as allergies, fibrosis, and metabolic diseases.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11616624/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142768187","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}
Amir Ferry, Kianoosh M Mempel, Alexander Monell, Miguel Reina-Campos, Nicole E Scharping, Maximilian Heeg, Kennidy K Takehara, Shiruyeh Schokrpur, Ning Kuo, Robert Saddawi-Konefka, J Silvio Gutkind, Ananda W Goldrath
{"title":"The XCL1-XCR1 axis supports intestinal tissue residency and antitumor immunity.","authors":"Amir Ferry, Kianoosh M Mempel, Alexander Monell, Miguel Reina-Campos, Nicole E Scharping, Maximilian Heeg, Kennidy K Takehara, Shiruyeh Schokrpur, Ning Kuo, Robert Saddawi-Konefka, J Silvio Gutkind, Ananda W Goldrath","doi":"10.1084/jem.20240776","DOIUrl":"10.1084/jem.20240776","url":null,"abstract":"<p><p>Tissue-resident memory T cells (TRM) provide frontline protection against pathogens and emerging malignancies. Tumor-infiltrating lymphocytes (TIL) with TRM features are associated with improved clinical outcomes. However, the cellular interactions that program TRM differentiation and function are not well understood. Using murine genetic models and targeted spatial transcriptomics, we found that the CD8+ T cell-derived chemokine XCL1 is critical for TRM formation and conventional DC1 (cDC1) supported the positioning of intestinal CD8+ T cells during acute viral infection. In tumors, enforced Xcl1 expression by antigen-specific CD8+ T cells promoted intratumoral cDC1 accumulation and T cell persistence, leading to improved overall survival. Notably, analysis of human TIL and TRM revealed conserved expression of XCL1 and XCL2. Thus, we have shown that the XCL1-XCR1 axis plays a non-cell autonomous role in guiding intestinal CD8+ TRM spatial differentiation and tumor control.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 2","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143006489","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}
{"title":"RNase T2 deficiency promotes TLR13-dependent replenishment of tissue-protective Kupffer cells.","authors":"Ryota Sato, Kaiwen Liu, Takuma Shibata, Katsuaki Hoshino, Kiyoshi Yamaguchi, Toru Miyazaki, Ryosuke Hiranuma, Ryutaro Fukui, Yuji Motoi, Yuri Fukuda-Ohta, Yun Zhang, Tatjana Reuter, Yuko Ishida, Toshikazu Kondo, Tomoki Chiba, Hiroshi Asahara, Masato Taoka, Yoshio Yamauchi, Toshiaki Isobe, Tsuneyasu Kaisho, Yoichi Furukawa, Eicke Latz, Kohta Nakatani, Yoshihiro Izumi, Yunzhong Nie, Hideki Taniguchi, Kensuke Miyake","doi":"10.1084/jem.20230647","DOIUrl":"10.1084/jem.20230647","url":null,"abstract":"<p><p>Lysosomal stress due to the accumulation of nucleic acids (NAs) activates endosomal TLRs in macrophages. Here, we show that lysosomal RNA stress, caused by the lack of RNase T2, induces macrophage accumulation in multiple organs such as the spleen and liver through TLR13 activation by microbiota-derived ribosomal RNAs. TLR13 triggered emergency myelopoiesis, increasing the number of myeloid progenitors in the bone marrow and spleen. Splenic macrophages continued to proliferate and mature into macrophages expressing the anti-inflammatory cytokine IL-10. In the liver, TLR13 activated monocytes/macrophages to proliferate and mature into monocyte-derived KCs (moKCs), in which, the liver X receptor (LXR) was activated. In accumulated moKCs, tissue clearance genes such as MerTK, AXL, and apoptosis inhibitor of macrophage (AIM) were highly expressed, while TLR-dependent production of proinflammatory cytokines was impaired. Consequently, Rnaset2-/- mice were resistant to acute liver injuries elicited by acetaminophen (APAP) and LPS with D-galactosamine. These findings suggest that TLR13 activated by lysosomal RNA stress promotes the replenishment of tissue-protective Kupffer cells.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032940","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}
{"title":"Autocrine TGF-β1 drives tissue-specific differentiation and function of resident NK cells.","authors":"Colin Sparano, Darío Solís-Sayago, Nathan Sébastien Zangger, Lukas Rindlisbacher, Hannah Van Hove, Marijne Vermeer, Frederike Westermann, Caroline Mussak, Elisa Rallo, Stanislav Dergun, Gioana Litscher, Yishu Xu, Mitchell Bijnen, Christin Friedrich, Melanie Greter, Vanda Juranić Lisnić, Burkhard Becher, Georg Gasteiger, Annette Oxenius, Sonia Tugues","doi":"10.1084/jem.20240930","DOIUrl":"10.1084/jem.20240930","url":null,"abstract":"<p><p>Group 1 innate lymphoid cells (ILCs) encompass NK cells and ILC1s, which have non-redundant roles in host protection against pathogens and cancer. Despite their circulating nature, NK cells can establish residency in selected tissues during ontogeny, forming a distinct functional subset. The mechanisms that initiate, maintain, and regulate the conversion of NK cells into tissue-resident NK (trNK) cells are currently not well understood. Here, we identify autocrine transforming growth factor-β (TGF-β) as a cell-autonomous driver for NK cell tissue residency across multiple glandular tissues during development. Cell-intrinsic production of TGF-β was continuously required for the maintenance of trNK cells and synergized with Hobit to enhance cytotoxic function. Whereas autocrine TGF-β was redundant in tumors, our study revealed that NK cell-derived TGF-β allowed the expansion of cytotoxic trNK cells during local infection with murine cytomegalovirus (MCMV) and contributed to viral control in the salivary gland. Collectively, our findings reveal tissue-specific regulation of trNK cell differentiation and function by autocrine TGF-β1, which is relevant for antiviral immunity.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11654236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142846689","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}
{"title":"Tissue-resident NK cells do their own glandscaping.","authors":"Jacob A Myers, Shanelle P Reilly, Laurent Brossay","doi":"10.1084/jem.20242253","DOIUrl":"10.1084/jem.20242253","url":null,"abstract":"<p><p>In this issue of JEM, Sparano et al. (https://doi.org/10.1084/jem.20240930) present compelling evidence that salivary gland trNK cells originate from cNK cells and are developmentally distinct from ILC1 cells. Mechanistically, they demonstrate that continuous autocrine TGF-β signaling drives salivary gland tissue residency and works in synergy with IL-15 to enhance Hobit-dependent cytotoxicity.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 3","pages":""},"PeriodicalIF":12.6,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697971/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921243","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}
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
