Evidence map›Paper›PMID 42774178›Full record

ArticleFrontiers in immunology2026

IFN-γ-dominant immune shift is associated with reduced protective ILC2 responses in chronic kidney disease.

Yoshihiro Kuno, Hiroki Ishikawa, Ryuichi Nagashima, Yasunari Matsuzaka, Chikara Kohda, Nobuhiro Kanazawa, Taihei Suzuki, Takeo Isozaki, Hirotaka Kuwata, Masayuki Iyoda

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Yoshihiro Kuno *Department of Microbiology and Immunology, Showa Medical University Graduate School of Medicine, Tokyo, Japan.
Hiroki Ishikawa *Department of Microbiology and Immunology, Showa Medical University Graduate School of Medicine, Tokyo, Japan.
Ryuichi NagashimaDepartment of Microbiology and Immunology, Showa Medical University Graduate School of Medicine, Tokyo, Japan.
Yasunari MatsuzakaDepartment of Microbiology and Immunology, Showa Medical University Graduate School of Medicine, Tokyo, Japan.
Chikara KohdaDepartment of Microbiology and Immunology, Showa Medical University Graduate School of Medicine, Tokyo, Japan.
Nobuhiro KanazawaDivision of Nephrology, Department of Medicine, Showa Medical University Graduate School of Medicine, Tokyo, Japan.
Taihei SuzukiDivision of Nephrology, Department of Medicine, Showa Medical University Graduate School of Medicine, Tokyo, Japan.
Takeo IsozakiDepartment of Pathogenesis and Translational Medicine, Showa Medical University Graduate School of Pharmacy, Tokyo, Japan.
Hirotaka KuwataDepartment of Oral Microbiology and Immunology, Showa Medical University Graduate School of Dentistry, Tokyo, Japan.
Masayuki IyodaDepartment of Microbiology and Immunology, Showa Medical University Graduate School of Medicine, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) progression is driven by an imbalance between inflammatory injury and tissue repair; however, the immune mechanisms that disrupt reparative pathways remain incompletely understood. Group 2 innate lymphoid cells (ILC2s) play protective roles in epithelial integrity and antifibrotic responses in the kidney, yet the signals that limit their maintenance during chronic inflammation are unclear. In this study, we investigated whether interferon-γ (IFN-γ)-dominant immune polarization is associated with the loss of renal ILC2s and exacerbation of CKD. Using a murine model of adenine-induced CKD, administration of α-galactosylceramide (αGalCer), a glycolipid known to activate invariant NKT cells, exacerbated renal dysfunction and tubulointerstitial injury. This was accompanied by enhanced inflammatory responses and a shift toward a type 1-dominant immune milieu. Notably, αGalCer treatment was associated with reduced renal ILC2 and regulatory T cell abundance, along with suppression of type 2 cytokines. Time-course analysis revealed a rapid and transient increase in renal

Indexed as

Immunity, InnateInterferon-gammaLymphocytesRenal Insufficiency, ChronicAnimalsCytokinesDisease Models, AnimalGalactosylceramidesKidneyMaleMiceMice, Inbred C57BLNatural Killer T-Cellsalpha-galactosylceramideCytokinesGalactosylceramidesInterferon-gammaCKDfibrosisIFN-γILC2NKT cells

Identifiers

PMID42774178
PMCPMC13593754

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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.