Evidence map›Paper›PMID 41100157›Full record

ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2026

Plasmacytoid dendritic cells modulate the production of mucosal IgA in IgA nephropathy.

Yusuke Fukao, Hitoshi Suzuki, Yoshihito Nihei, Yuko Makita, Toshiki Kano, Maiko Nakayama, Mingfeng Lee, Rina Kato, Masao Kihara, Yusuke Suzuki

Abstract read
In one paragraph

Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2026. 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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
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

10 authors.

Yusuke FukaoDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Hitoshi SuzukiDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Yoshihito NiheiDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Yuko MakitaDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Toshiki KanoDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Maiko NakayamaDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Mingfeng LeeDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Rina KatoDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Masao KiharaDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Yusuke SuzukiDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.ORCID 0000-0002-4077-9747

Funding

JSPS 20K08643
6 · The paper itself

Abstract

background and hypothesisAberrantly glycosylated immunoglobulin A (IgA) plays a central role in the pathogenesis of IgA nephropathy (IgAN). The activation of Toll-like receptor 9 (TLR9) has been shown to induce aberrant glycosylation of IgA via the a proliferation-inducing ligand (APRIL)-mediated pathway. TLR9 is known to be highly expressed in B cells and plasmacytoid dendritic cells (pDCs). Although the stimulation of TLR9 in B cells has been reported to promote the production of aberrantly glycosylated IgA, the effects of TLR9 stimulation on pDCs remain unclear. Therefore, in this study, we focused on the role of mucosal pDCs in the synthesis of aberrantly glycosylated IgA in patients with IgAN.

methodsWe evaluated the distribution of the DC subsets in tonsillar mononuclear cells (MNCs). The synthesis of aberrantly glycosylated IgA in MNCs cultured with or without pDCs was analyzed. We also evaluated the effects of pDC depletion on the production of aberrantly glycosylated IgA in ddY mice, a spontaneous murine model of IgAN, nasally immunized with CpG-oligonucleotide, a ligand for TLR9.

resultsThe percentage of DCs, especially pDCs, was significantly higher in the palatine tonsils of patients with IgAN than in those of patients with chronic tonsillitis. In patients with IgAN, the abundance of pDCs was significantly correlated with the APRIL and TLR9 expressions in tonsillar MNCs. The levels of aberrantly glycosylated IgA in culture supernatants of tonsillar MNCs were found to be increased in the presence of pDCs. The pDC-depleted ddY mice exhibited significantly lower serum levels of aberrantly glycosylated IgA in vivo.

conclusionMucosal pDCs contribute to the pathogenesis of IgAN by facilitating the production of aberrantly glycosylated IgA via TLR9 signaling. Our findings demonstrated that pDC may be a novel therapeutic target for IgAN.

Indexed as

Dendritic CellsGlomerulonephritis, IGAImmunoglobulin AMucous MembraneAdultAnimalsCells, CulturedFemaleGlycosylationHumansMaleMiceMiddle AgedOligodeoxyribonucleotidesPalatine TonsilToll-Like Receptor 9glycosylated IgAImmunoglobulin AOligodeoxyribonucleotidesTLR9 protein, humanToll-Like Receptor 9Tumor Necrosis Factor Ligand Superfamily Member 13APRILGd-IgA1IgA nephropathyplasmacytoid dendritic cellsTLR9

Identifiers

PMID41100157
PMCPMC13130947

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.