Evidence map›Paper›PMID 34813503›Full record

ArticleThe Journal of clinical investigation2022

CD153/CD30 signaling promotes age-dependent tertiary lymphoid tissue expansion and kidney injury.

Yuki Sato, Akiko Oguchi, Yuji Fukushima, Kyoko Masuda, Naoya Toriu, Keisuke Taniguchi, Takahisa Yoshikawa, Xiaotong Cui, Makiko Kondo, Takeshi Hosoi and 18 more

Open access · hybridAbstract readVideo-Audio Media
In one paragraph

Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Article
  3. Age-associated Autoimmunity Driven by T cell Immunosenescence.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. A CD4Nature communications · 2026
    Article
  8. Review
  9. Article
  10. Review
  11. The Aging Kidney and Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

9 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

28 authors at 7 institutions in 4 countries.

Yuki SatoDepartment of Nephrology.
Akiko OguchiDepartment of Nephrology.
Yuji FukushimaDepartment of Immunosenescence and.
Kyoko MasudaDepartment of Immunology, Institute for Frontier Medical Science, and.
Naoya ToriuDepartment of Nephrology.
Keisuke TaniguchiDepartment of Nephrology.
Takahisa YoshikawaDepartment of Nephrology.
Xiaotong CuiDepartment of Nephrology.
Makiko KondoDepartment of Nephrology.
Takeshi HosoiMedical Innovation Center TMK Project, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Shota KomidoriDepartment of Nephrology.
Yoko ShimizuDepartment of Nephrology.
Harumi FujitaDepartment of Immunology and Cell Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Li JiangDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Yingyi KongDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Takashi YamanashiMedical Sciences Innovation Hub Program, RIKEN, Tokyo, Japan.
Jun SeitaMedical Sciences Innovation Hub Program, RIKEN, Tokyo, Japan.
Takuya YamamotoInstitute for the Advanced Study of Human Biology (ASHBi), Kyoto University, Kyoto, Japan.
Shinya ToyokuniDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
Yoko HamazakiDepartment of Immunology and Cell Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masakazu HattoriDepartment of Immunosenescence and.
Yasunobu YoshikaiDivision of Host Defense, Network Center for Infectious Disease, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Peter BoorInstitute of Pathology and.
Jürgen FloegeDepartment of Nephrology, RWTH University of Aachen, Aachen, Germany.
Hiroshi KawamotoDepartment of Immunology, Institute for Frontier Medical Science, and.
Yasuhiro MurakawaRIKEN Center for Integrative Medical Sciences, Yokohama, Kanagawa, Japan.
Nagahiro MinatoDepartment of Immunology and Cell Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Motoko YanagitaDepartment of Nephrology.
Kyoto University · JPFrontier Medical College · PKNagoya University · JPRWTH Aachen University · DEKyushu University · JPRIKEN Center for Integrative Medical Sciences · JPThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tertiary lymphoid tissues (TLTs) facilitate local T and B cell interactions in chronically inflamed organs. However, the cells and molecular pathways that govern TLT formation are poorly defined. Here, we identified TNF superfamily CD153/CD30 signaling between 2 unique age-dependent lymphocyte subpopulations, CD153+PD-1+CD4+ senescence-associated T (SAT) cells and CD30+T-bet+ age-associated B cells (ABCs), as a driver for TLT expansion. SAT cells, which produced ABC-inducing factors IL-21 and IFN-γ, and ABCs progressively accumulated within TLTs in aged kidneys after injury. Notably, in kidney injury models, CD153 or CD30 deficiency impaired functional SAT cell induction, which resulted in reduced ABC numbers and attenuated TLT formation with improved inflammation, fibrosis, and renal function. Attenuated TLT formation after transplantation of CD153-deficient bone marrow further supported the importance of CD153 in immune cells. Clonal analysis revealed that SAT cells and ABCs in the kidneys arose from both local differentiation and recruitment from the spleen. In the synovium of aged rheumatoid arthritis patients, T peripheral helper/T follicular helper cells and ABCs also expressed CD153 and CD30, respectively. Together, our data reveal a previously unappreciated function of CD153/CD30 signaling in TLT formation and propose targeting the CD153/CD30 signaling pathway as a therapeutic target for slowing kidney disease progression.

Indexed as

Acute Kidney InjuryAgingAnimalsCD30 LigandCD4-Positive T-LymphocytesKi-1 AntigenLymphoid TissueMaleMiceMice, KnockoutSignal TransductionCD30 LigandKi-1 AntigenTnfsf8 protein, mouseChronic kidney diseaseInflammationNephrology

Identifiers

PMID34813503
PMCPMC8759786
OpenAlexW3217220006

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.