Evidence map›Paper›PMID 37462944›Full record

ArticleThe Journal of experimental medicine2023

TLR7/8 stress response drives histiocytosis in SLC29A3 disorders.

Takuma Shibata, Ryota Sato, Masato Taoka, Shin-Ichiroh Saitoh, Mayumi Komine, Kiyoshi Yamaguchi, Susumu Goyama, Yuji Motoi, Jiro Kitaura, Kumi Izawa and 22 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
12.8field-weighted citation impact, top 1% of its field
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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 22 citations in OpenAlex.

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  11. Endosomal Toll-Like Receptors as Therapeutic Targets for Autoimmune Diseases.Advances in experimental medicine and biology · 2024
    Article
4 · The record

Corrections and comments

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

32 authors at 11 institutions in 3 countries.

Takuma ShibataDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0009-0001-3013-4566
Ryota SatoDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0009-0002-8299-8363
Masato TaokaDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Tokyo, Japan.ORCID 0000-0001-5554-4951
Shin-Ichiroh SaitohDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-1403-2260
Mayumi KomineDepartment of Dermatology, Jichi Medical University, Tochigi, Japan.ORCID 0000-0002-1086-1803
Kiyoshi YamaguchiDivision of Clinical Genome Research, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0003-2113-4369
Susumu GoyamaDivision of Molecular Oncology, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-9339-1826
Yuji MotoiDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0009-0001-1272-0502
Jiro KitauraAtopy Research Center, Graduate School of Medicine, Juntendo University , Tokyo, Japan.ORCID 0000-0002-5083-8368
Kumi IzawaAtopy Research Center, Graduate School of Medicine, Juntendo University , Tokyo, Japan.ORCID 0000-0003-4746-7225
Yoshio YamauchiDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Tokyo, Japan.ORCID 0009-0007-5544-7415
Yumiko TsukamotoDepartment of Mycobacteriology, Leprosy Research Center, National Institute of Infectious Diseases, Tokyo, Japan.ORCID 0000-0001-6045-4328
Takeshi IchinoheDivision of Viral Infection, Department of Infectious Disease Control, International Research Center for Infectious Diseases, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-6376-2841
Etsuko FujitaDepartment of Dermatology, Jichi Medical University, Tochigi, Japan.ORCID 0009-0000-3712-9551
Ryosuke HiranumaDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0009-0000-7234-6762
Ryutaro FukuiDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-5263-509X
Yoichi FurukawaDivision of Clinical Genome Research, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0003-0462-8631
Toshio KitamuraDivision of Cellular Therapy, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-7855-1767
Toshiyuki TakaiDepartment of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.ORCID 0000-0002-4549-7116
Arinobu TojoDepartment of Hematology and Oncology, Research Hospital, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-9016-1948
Mamitaro OhtsukiDepartment of Dermatology, Jichi Medical University, Tochigi, Japan.ORCID 0000-0001-7845-6698
Umeharu OhtoGraduate School of Pharmaceutical Sciences, The University of Tokyo , Tokyo, Japan.ORCID 0000-0002-4422-4044
Toshiyuki ShimizuGraduate School of Pharmaceutical Sciences, The University of Tokyo , Tokyo, Japan.ORCID 0000-0002-0547-8922
Manabu OzawaLaboratory of Developmental Genetics, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo , Tokyo, Japan.ORCID 0000-0003-3284-7161
Nobuaki YoshidaLaboratory of Developmental Genetics, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo , Tokyo, Japan.ORCID 0009-0004-5335-6550
Toshiaki IsobeDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Tokyo, Japan.ORCID 0000-0002-0934-9298
Eicke LatzInstitute of Innate Immunity, University Hospital Bonn, University of Bonn , Bonn, Germany.ORCID 0000-0003-1488-5666
Kojiro MukaiDepartment of Integrative Life Sciences, Laboratory of Organelle Pathophysiology, Graduate School of Life Sciences, Tohoku University, Sendai, Japan.ORCID 0000-0001-9806-910X
Tomohiko TaguchiDepartment of Integrative Life Sciences, Laboratory of Organelle Pathophysiology, Graduate School of Life Sciences, Tohoku University, Sendai, Japan.ORCID 0000-0003-0464-6370
Hiroaki HemmiLaboratory of Immunology, Faculty of Veterinary Medicine, Okayama University of Science , Imabari, Japan.ORCID 0009-0000-0938-0618
Shizuo AkiraLaboratory of Host Defense, World Premier Institute-Immunology Frontier Research Center (WPI-IFReC), Osaka University , Osaka, Japan.ORCID 0000-0001-7602-9617
Kensuke MiyakeDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-6629-226X
The University of Tokyo · JPJichi Medical University · JPTohoku University · JPTokyo Medical University · JPTokyo Metropolitan University · JPJuntendo University · JPNational Institute of Infectious Diseases · JPOkayama University of Science · JPOsaka International University · JPTokyo Medical University Hospital · JPUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss-of-function mutations in the lysosomal nucleoside transporter SLC29A3 cause lysosomal nucleoside storage and histiocytosis: phagocyte accumulation in multiple organs. However, little is known about the mechanism by which lysosomal nucleoside storage drives histiocytosis. Herein, histiocytosis in Slc29a3-/- mice was shown to depend on Toll-like receptor 7 (TLR7), which senses a combination of nucleosides and oligoribonucleotides (ORNs). TLR7 increased phagocyte numbers by driving the proliferation of Ly6Chi immature monocytes and their maturation into Ly6Clow phagocytes in Slc29a3-/- mice. Downstream of TLR7, FcRγ and DAP10 were required for monocyte proliferation. Histiocytosis is accompanied by inflammation in SLC29A3 disorders. However, TLR7 in nucleoside-laden splenic monocytes failed to activate inflammatory responses. Enhanced production of proinflammatory cytokines was observed only after stimulation with ssRNAs, which would increase lysosomal ORNs. Patient-derived monocytes harboring the G208R SLC29A3 mutation showed enhanced survival and proliferation in a TLR8-antagonist-sensitive manner. These results demonstrated that TLR7/8 responses to lysosomal nucleoside stress drive SLC29A3 disorders.

Indexed as

HistiocytosisToll-Like Receptor 7AnimalsCytokinesMembrane GlycoproteinsMiceMutationNucleosidesNucleoside Transport ProteinsToll-Like Receptor 8CytokinesMembrane GlycoproteinsNucleosidesNucleoside Transport ProteinsSlc29a3 protein, mouseTlr7 protein, mouseTLR8 protein, mouseToll-Like Receptor 7Toll-Like Receptor 8

Identifiers

PMID37462944
PMCPMC10354536
OpenAlexW4384627457

What OpenQuestion holds

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Registered trials

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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.