Evidence map›Paper›PMID 40269956›Full record

ArticleArthritis research & therapy2025

Exhausted natural killer cells in adult IgA vasculitis.

Matija Bajželj, Emanuela Senjor, Nika Boštic, Matjaž Hladnik, Snežna Sodin-Šemrl, Milica Perišić Nanut, Janko Kos, Alojz Ihan, Alojzija Hočevar, Andreja Nataša Kopitar and 1 more

Abstract read
In one paragraph

Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Matija BajželjDepartment of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Emanuela SenjorDepartment of Biotechnology, Jožef Stefan Institute, Ljubljana, Slovenia.
Nika BošticDepartment of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Matjaž HladnikFaculty of Mathematics, Natural Sciences and Information Technologies, University of Primorska, Koper, Slovenia.
Snežna Sodin-ŠemrlDepartment of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Milica Perišić NanutDepartment of Biotechnology, Jožef Stefan Institute, Ljubljana, Slovenia.
Janko KosDepartment of Biotechnology, Jožef Stefan Institute, Ljubljana, Slovenia.
Alojz IhanFaculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
Alojzija HočevarDepartment of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Andreja Nataša Kopitar *Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.
Katja Lakota *Department of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia. katja.lakota@kclj.si.

Funding

The Slovenian Research and Innovation Agency J7-60132The Slovenian Research and Innovation Agency P3-0314
6 · The paper itself

Abstract

introductionIgA vasculitis nephritis (IgAVN) manifests in up to 84% of adult patients with IgA vasculitis (IgAV) and is associated with an elevated risk of progression to chronic kidney failure. The underlying pathogenic mechanism of adult IgAVN in leukocytes remain largely uncharacterised. Although natural killer (NK) cells were investigated in paediatric IgAV, their specific role in the pathogenesis of adult IgAV has yet to be elucidated.

methodsRNA sequencing of leukocytes from adult IgAV patients and healthy controls (HC) was performed. NK cells' cytotoxicity was assessed using calcein-AM stained K562 cells, and exocytosis was measured by LAMP-1/CD107a expression. Intracellular perforin and granzyme B were analyzed via flow cytometry, and cytokine secretion was measured by Luminex xMAP. Interferon-induced genes were validated with qPCR.

resultsPrincipal component analysis (PCA) of leukocyte gene expression profiles distinguished IgAV patients from HC. Pathway enrichment analysis showed differences in patients' subsets - Interferon signalling Reactome pathway was observed only in sample from patients with skin-limited IgAV (sl-IgAV) and was confirmed by increased expression of interferon-induced genes using qPCR. Only in samples from IgAVN patients enrichment of NK cell-mediated cytotoxicity KEGG pathway was found. NK cells from IgAVN patients showed significantly decreased cytotoxicity compared to samples from sl-IgAV patients (p = 2.53 × 10

conclusionPatients with IgAVN exhibited impaired cytotoxic and immunomodulatory functions of NK cells, along with a marked absence of interferon signaling in PBMCs. Further studies are needed to confirm if discrimination of patient subsets based on leukocyte samples might be of clinical use and if deregulated NK function might contribute to the pathogenesis of nephritis in adult IgAV.

Indexed as

Immunoglobulin AKiller Cells, NaturalVasculitisAdultFemaleHumansK562 CellsMaleMiddle AgedPerforinYoung AdultImmunoglobulin APerforinAdultsIgA vasculitisNatural killer cellsNephritisRNA sequencing

Identifiers

PMID40269956
PMCPMC12016069

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