Peptide-based vaccine targeting IL17A attenuates experimental spondyloarthritis in HLA-B27 transgenic rats.
Autoimmunity
Spondylitis, Ankylosing
Vaccination
Journal
RMD open
ISSN: 2056-5933
Titre abrégé: RMD Open
Pays: England
ID NLM: 101662038
Informations de publication
Date de publication:
02 2023
02 2023
Historique:
received:
09
11
2022
accepted:
19
01
2023
entrez:
3
2
2023
pubmed:
4
2
2023
medline:
8
2
2023
Statut:
ppublish
Résumé
Spondyloarthritis (SpA) is known as series of immune-mediated inflammatory disease of the axial and peripheral joints. Human leucocyte antigen (HLA)-B27 is a genetic risk factor for SpA. Recent evidence suggests that the interleukin -17 (IL17) axis strongly contributes to SpA. This study aimed to assess the efficacy of an IL17A peptide-based vaccine on SpA manifestations in model rats. HLA-B27/human β The IL17A peptide-based vaccine with alum adjuvant successfully induced antibody production and suppressed the arthritis score and joint thickness. X-ray and histological analyses showed that enthesitis, bone destruction and new bone formation were inhibited by the IL17A vaccine. The ELISpot assay showed that the IL17A peptide-based vaccine did not elicit any IL17A-reactive T cell responses. IL17A vaccine tends to mitigate, but not significant, in SpA treatment model. These data showed that the peptide-based vaccine targeting IL17A alleviated the SpA phenotype in a heat-inactivated MT-induced SpA model in HLA-B27/hβ IL17A peptide-based vaccine may be a therapeutic option for SpA treatment.
Identifiants
pubmed: 36737108
pii: rmdopen-2022-002851
doi: 10.1136/rmdopen-2022-002851
pmc: PMC9900070
pii:
doi:
Substances chimiques
aluminum sulfate
34S289N54E
HLA-B27 Antigen
0
Alum Compounds
0
IL17A protein, human
0
Interleukin-17
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: The Department of Health Development and Medicine is an endowed department that is supported by AnGes, Daicel, and FunPep. The Department of Clinical Gene Therapy is financially supported by Novartis, AnGes, Shionogi, Boeringher, Fancl, Saisei Mirai Clinics, Rohto, and FunPep. HN is a scientific advisor of Funpep. AT, MT, SK, TE, RA, MS, HT and RM are employers and stockholders of Funpep. The funder provided support in the form of salaries for authors but did not have any additional role in the study design, data analysis, decision to publish, or preparation of this manuscript. All other authors declare no competing interests.
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