Abstrakti
High carrier prevalence of STAT3 SH2 domain somatic mutations was recently discovered in CD8+ T cells. We found these low-allele-fraction clones in 26% of donors, without difference between multiple sclerosis (MS) patients and controls. Here we tested whether anti-viral antibodies associate with the carriership of these mutant clones. We compared antibody responses against common viruses in mutation carriers vs. non-carriers. Plasma samples of 152 donors (92 MS patients, 60 controls) were analyzed for antibodies against cytomegalovirus (CMV), Epstein-Barr virus (EBV), human herpesvirus-6A and parvovirus B19. The mutation carrier status associated with EBV VCA IgG level (p = 0.005) and remained significant after logistic regression (p = 0.036). This association was contributed similarly by MS patients and controls. These results suggest that EBV contributes to the generation or growth of these clones. The pathogenic role of the STAT3 mutant clones in MS is presently unclear, but their detailed characterization warrants further study.
Alkuperäiskieli | englanti |
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Artikkeli | 109733 |
Lehti | Clinical Immunology |
Vuosikerta | 255 |
Sivumäärä | 5 |
ISSN | 1521-6616 |
DOI - pysyväislinkit | |
Tila | Julkaistu - lokak. 2023 |
OKM-julkaisutyyppi | A1 Alkuperäisartikkeli tieteellisessä aikakauslehdessä, vertaisarvioitu |
Lisätietoja
Funding Information:The authors wish to thank all participants for the blood samples, CSC – IT Center for Science, Finland, for computational resources, and HUSLAB for virus antibody analyses. We thank the team 1 at HUS Diagnostic Center for excellent technical assistance. This study has been financially supported by research grants from the Helsinki University Hospital, University of Helsinki , the Multiple Sclerosis Foundation of Finland, the Finnish Cultural Foundation , Sigrid Juselius Foundation, Biogen Finland, Sanofi-Genzyme, Roche and Novartis. The funders had no role in study design, data collection or analysis.
Funding Information:
The authors wish to thank all participants for the blood samples, CSC – IT Center for Science, Finland, for computational resources, and HUSLAB for virus antibody analyses. We thank the team 1 at HUS Diagnostic Center for excellent technical assistance. This study has been financially supported by research grants from the Helsinki University Hospital, University of Helsinki, the Multiple Sclerosis Foundation of Finland, the Finnish Cultural Foundation, Sigrid Juselius Foundation, Biogen Finland, Sanofi-Genzyme, Roche and Novartis. The funders had no role in study design, data collection or analysis.
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