Article in The Journal of experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
27 authors.
Ryota SatoDivision of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0009-0002-8299-8363
Kaiwen LiuDivision of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0000-0002-0242-3838
Takuma ShibataDivision of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0009-0001-3013-4566
Katsuaki HoshinoDepartment of Immunology, Faculty of Medicine, Kagawa University, Miki, Japan.ORCID 0000-0003-0493-4815
Kiyoshi YamaguchiDivision of Clinical Genome Research, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0000-0003-2113-4369
Ryosuke HiranumaDivision of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0009-0000-7234-6762
Ryutaro FukuiDivision of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0000-0001-5263-509X
Yuji MotoiDivision of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0009-0001-1272-0502
Yuri Fukuda-OhtaDepartment of Immunology, Institute of Advanced Medicine, Wakayama Medical University, Kimiidera, Japan.ORCID 0009-0003-2779-1009
Yun ZhangDivision of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0009-0006-6813-7806
Tatjana ReuterInstitute of Innate Immunity, University Hospital Bonn, University of Bonn , Bonn, Germany.ORCID 0009-0003-5867-1683
Yuko IshidaDepartment of Forensic Medicine, Wakayama Medical University, Kimiidera, Japan.ORCID 0000-0001-6104-7599
Toshikazu KondoDepartment of Forensic Medicine, Wakayama Medical University, Kimiidera, Japan.ORCID 0000-0002-5059-8309
Tomoki ChibaDepartment of Systems Biomedicine, Tokyo Medical and Dental University, Bunkyo-ku, Japan.ORCID 0000-0001-5472-9030
Hiroshi AsaharaDepartment of Systems Biomedicine, Tokyo Medical and Dental University, Bunkyo-ku, Japan.ORCID 0000-0002-5215-8745
Masato TaokaDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Tokyo, Japan.ORCID 0000-0001-5554-4951
Yoshio YamauchiDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Tokyo, Japan.ORCID 0009-0007-5544-7415
Toshiaki IsobeDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Tokyo, Japan.ORCID 0000-0002-0934-9298
Tsuneyasu KaishoLaboratory for Inflammatory Regulation, RIKEN Center for Integrative Medical Science (IMS-RCAI), Yokohama, Japan.ORCID 0000-0003-2616-1665
Yoichi FurukawaDivision of Clinical Genome Research, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0000-0003-0462-8631
Eicke LatzInstitute of Innate Immunity, University Hospital Bonn, University of Bonn , Bonn, Germany.ORCID 0000-0003-1488-5666
Kohta NakataniDivision of Metabolomics, Medical Institute of Bioregulation, Kyushu University, Higashi-ku, Japan.ORCID 0000-0002-8270-6829
Yoshihiro IzumiDivision of Metabolomics, Medical Institute of Bioregulation, Kyushu University, Higashi-ku, Japan.ORCID 0000-0003-4608-4652
Yunzhong NieDivision of Regenerative Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0000-0002-1252-8326
Hideki TaniguchiDivision of Regenerative Medicine, Center for Stem Cell Biology and Regenerative Medicine, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0000-0002-6186-9266
Kensuke MiyakeDivision of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.ORCID 0000-0001-6629-226X
Funding
Daiichi Sankyo Foundation of Life ScienceJapan Agency for Medical Research and Development JP 20ek0109385Japan Society for the Promotion of Science JP 21H04800JST CREST JPMJCR21E4Ministry of Education, Culture, Sports, Science and TechnologyMochida Memorial Foundation for Medical and Pharmaceutical ResearchTakeda Science FoundationUehara FoundationUniversity of TokyoUniversity of Tokyo Pandemic Preparedness, Infection and Advanced Research Center
6 · The paper itself
Abstract
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.
Indexed as
EndoribonucleasesKupffer CellsToll-Like ReceptorsAcetaminophenAnimalsChemical and Drug Induced Liver InjuryCytokinesLiverLysosomesMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutSpleenAcetaminophenCytokinesEndoribonucleasesToll-Like Receptors
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
RNase T2 deficiency promotes TLR13-dependent replenishment of tissue-protective Kupffer cells. · full record | OpenQuestion