DNA vaccine encoding heat shock protein 90 protects from murine lupus.


Journal

Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438

Informations de publication

Date de publication:
22 06 2020
Historique:
received: 07 02 2020
accepted: 12 06 2020
entrez: 24 6 2020
pubmed: 24 6 2020
medline: 22 6 2021
Statut: epublish

Résumé

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the presence of autoantibodies to multiple self-antigens, including heat shock proteins (HSP). Because of the increased expression of HSP90 and abnormal immune responses to it in SLE, we investigated whether an HSP90 DNA vaccine could modulate the development and clinical manifestations of SLE in lupus-prone mice. (NZB x NZW)F Vaccination with HSP90 DNA reduced lupus disease manifestations and prolonged the survival of NZB/W mice. The protective effects of the HSP90 DNA vaccine associated with the induction of tolerogenic dendritic cells (DCs) and an expansion of T regulatory cells (Tregs). The beneficial effects of DNA vaccination with HSP90 in murine SLE support the possibility of HSP90-based therapeutic modalities of intervention in SLE.

Sections du résumé

BACKGROUND
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the presence of autoantibodies to multiple self-antigens, including heat shock proteins (HSP). Because of the increased expression of HSP90 and abnormal immune responses to it in SLE, we investigated whether an HSP90 DNA vaccine could modulate the development and clinical manifestations of SLE in lupus-prone mice.
METHODS
(NZB x NZW)F
RESULTS
Vaccination with HSP90 DNA reduced lupus disease manifestations and prolonged the survival of NZB/W mice. The protective effects of the HSP90 DNA vaccine associated with the induction of tolerogenic dendritic cells (DCs) and an expansion of T regulatory cells (Tregs).
CONCLUSIONS
The beneficial effects of DNA vaccination with HSP90 in murine SLE support the possibility of HSP90-based therapeutic modalities of intervention in SLE.

Identifiants

pubmed: 32571400
doi: 10.1186/s13075-020-02246-4
pii: 10.1186/s13075-020-02246-4
pmc: PMC7310240
doi:

Substances chimiques

Autoantibodies 0
Heat-Shock Proteins 0
Vaccines, DNA 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

152

Subventions

Organisme : NICHD NIH HHS
ID : R21 HD097531
Pays : United States
Organisme : NIH HHS
ID : HD097531
Pays : United States

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Auteurs

Aijing Liu (A)

Department of Medicine, University of California Los Angeles, Los Angeles, CA, 90095, USA.
Present Address: Second Hospital of Hebei Medical University, Shijiazhuang, China.

Fu-Dong Shi (FD)

Barrow Neurological Institute, Phoenix, AZ, 85013, USA.

Irun R Cohen (IR)

Department of Immunology, The Weizmann Institute of Science, 7610001, Rehovot, Israel.

Giuseppe Castaldo (G)

Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Federico II University of Naples, Naples, 80131, Italy.

Giuseppe Matarese (G)

Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Federico II University of Naples, Naples, 80131, Italy.
Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, 80131, Italy.

Francisco J Quintana (FJ)

Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.

Antonio La Cava (A)

Department of Medicine, University of California Los Angeles, Los Angeles, CA, 90095, USA. alacava@mednet.ucla.edu.

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Classifications MeSH