Same, Same, but Different-Whole Blood Transcriptomes of ANCA-Associated Vasculitis and Giant Cell Arteritis.
5 affiliations
- 1Department of Rheumatology and Immunology, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.
- 2Graduate School for Health Sciences, University of Bern, 3010 Bern, Switzerland.
- 3Interfaculty Bioinformatics Unit, University of Bern, 3010 Bern, Switzerland.
- 4Department of Internal Medicine with a Course in Cardiology and Rheumatology, Bogomolets National Medical University, 01601 Kyiv, Ukraine.
- 5Department for Biomedical Research, University of Bern, 3010 Bern, Switzerland.
Abstract
ANCA-associated small vessel vasculitis (AAV) and giant cell arteritis (GCA) are two clinically distinct forms of vasculitides with a high risk of relapse. We aimed to evaluate and compare the role of immune cells in patients with both vasculitis subtypes with active disease. Whole blood was collected from 12 untreated newly diagnosed or relapsing patients with AAV, 10 untreated newly diagnosed patients with GCA, and 11 age- and sex-matched healthy controls (HC). Transcriptomes were analysed by RNA sequencing. Differentially expressed genes (DEG) were calculated across disease groups. Pathway enrichment analysis was conducted using Overrepresentation Analysis (ORA), and Gene Onthology and Gene Set Enrichment Analysis (GSEA). The platelet receptor component CD42a was assessed by flow cytometry. We identified 104 DEG in AAV compared to HC, and 504 DEG between GCA and HC in whole blood samples. Strikingly, only 19 genes were differentially expressed between AAV and GCA. ORA of DEG, distinguishing both vasculitis subtypes from HC, identified pathways exclusively involved in innate immunity. GSEA of both AAV and GCA versus HC pointed to a striking overlap in up-regulated pathways comprising seven out of ten top signalling pathways, including "IL6 JAK Stat3 signalling", "TNF signalling" and "complement activation". We detected increased levels of CD42a on platelets of patients with GCA, in line with an increased expression of platelet-associated genes in GCA compared to AAV. Our results suggest that the rather homogeneous transcriptome of circulating immune cells does not sufficiently explain the clinically distinct phenotypes of AAV and GCA.
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BibTeX
@article{amsler2026same,
title = {{Same, Same, but Different-Whole Blood Transcriptomes of ANCA-Associated Vasculitis and Giant Cell Arteritis.}},
author = {Jennifer Amsler and Marco Kreuzer and Liubov Petelytska and Sara Andrea Krättli and Oleg Iaremenko and Matthias Brunner and Daniel Guggisberg and Lisa Christ and Matthias Gasser and Fabio Ryser and Adela Sarbu and Luca Seitz and Pascal Seitz and Britta Maurer and Kerstin Klein},
journal = {International journal of molecular sciences},
year = {2026},
month = sep,
doi = {10.3390/ijms27198513},
url = {https://europepmc.org/article/MED/42883764},
note = {CC BY},
}
RIS
TY - JOUR
TI - Same, Same, but Different-Whole Blood Transcriptomes of ANCA-Associated Vasculitis and Giant Cell Arteritis.
AU - Jennifer Amsler
AU - Marco Kreuzer
AU - Liubov Petelytska
AU - Sara Andrea Krättli
AU - Oleg Iaremenko
AU - Matthias Brunner
AU - Daniel Guggisberg
AU - Lisa Christ
AU - Matthias Gasser
AU - Fabio Ryser
AU - Adela Sarbu
AU - Luca Seitz
AU - Pascal Seitz
AU - Britta Maurer
AU - Kerstin Klein
PY - 2026
DA - 2026/09/24
JO - International journal of molecular sciences
DO - 10.3390/ijms27198513
UR - https://europepmc.org/article/MED/42883764
AB - ANCA-associated small vessel vasculitis (AAV) and giant cell arteritis (GCA) are two clinically distinct forms of vasculitides with a high risk of relapse. We aimed to evaluate and compare the role of immune cells in patients with both vasculitis subtypes with active disease. Whole blood was collected from 12 untreated newly diagnosed or relapsing patients with AAV, 10 untreated newly diagnosed patients with GCA, and 11 age- and sex-matched healthy controls (HC). Transcriptomes were analysed by RNA sequencing. Differentially expressed genes (DEG) were calculated across disease groups. Pathway enrichment analysis was conducted using Overrepresentation Analysis (ORA), and Gene Onthology and Gene Set Enrichment Analysis (GSEA). The platelet receptor component CD42a was assessed by flow cytometry. We identified 104 DEG in AAV compared to HC, and 504 DEG between GCA and HC in whole blood samples. Strikingly, only 19 genes were differentially expressed between AAV and GCA. ORA of DEG, distinguishing both vasculitis subtypes from HC, identified pathways exclusively involved in innate immunity. GSEA of both AAV and GCA versus HC pointed to a striking overlap in up-regulated pathways comprising seven out of ten top signalling pathways, including "IL6 JAK Stat3 signalling", "TNF signalling" and "complement activation". We detected increased levels of CD42a on platelets of patients with GCA, in line with an increased expression of platelet-associated genes in GCA compared to AAV. Our results suggest that the rather homogeneous transcriptome of circulating immune cells does not sufficiently explain the clinically distinct phenotypes of AAV and GCA.
SN - 1422-0067
ER -