Belimumab Decreases Autophagy and Citrullination in Peripheral Blood Mononuclear Cells from Patients with Systemic Lupus Erythematosus.


Journal

Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052

Informations de publication

Date de publication:
13 01 2022
Historique:
received: 22 12 2021
accepted: 10 01 2022
entrez: 21 1 2022
pubmed: 22 1 2022
medline: 24 2 2022
Statut: epublish

Résumé

Belimumab (BLM) is a B lymphocyte stimulator (BLyS) inhibitor approved for the treatment of systemic lupus erythematosus (SLE). Autophagy is a cell survival mechanism involved in the pathogenesis of SLE. Citrullination is a post-translational modification catalyzed by peptidylarginine deiminase (PAD) enzymes. Autophagy and citrullination may generate neoepitopes, evoking an autoimmune response. No previous studies have investigated the connection of these processes, and how BLM could affect them, in SLE. Ex vivo autophagy and protein citrullination were analyzed by western blot in lysates from 26 SLE patients' PBMCs at baseline and after 2, 4, and 12 weeks of BLM administration, and from 16 healthy donors' PBMCs. Autophagic PBMCs were identified by the immunofluorescent detection of the autophagy-associated proteins LC3B (LC3 puncta) and LAMP-1. Autophagosome accumulation was evaluated in CD14

Identifiants

pubmed: 35053379
pii: cells11020262
doi: 10.3390/cells11020262
pmc: PMC8773843
pii:
doi:

Substances chimiques

Antibodies, Monoclonal, Humanized 0
Antigens, CD 0
B-Cell Activation Factor Receptor 0
B-Cell Maturation Antigen 0
Biomarkers 0
Interleukin-18 0
LAMP1 protein, human 0
Lysosomal Membrane Proteins 0
MAP1LC3A protein, human 0
Microtubule-Associated Proteins 0
TNFRSF13C protein, human 0
Transmembrane Activator and CAML Interactor Protein 0
belimumab 73B0K5S26A

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Fondazione Umberto Di Mario
ID : N/A

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Auteurs

Tania Colasanti (T)

Rheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico, 155, 00161 Rome, Italy.

Francesca Romana Spinelli (FR)

Rheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico, 155, 00161 Rome, Italy.

Cristiana Barbati (C)

Rheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico, 155, 00161 Rome, Italy.

Fulvia Ceccarelli (F)

Rheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico, 155, 00161 Rome, Italy.

Susanna Scarpa (S)

Department of Experimental Medicine, Sapienza University of Rome, Viale del Policlinico, 155, 00161 Rome, Italy.

Marta Vomero (M)

Rheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico, 155, 00161 Rome, Italy.

Cristiano Alessandri (C)

Rheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico, 155, 00161 Rome, Italy.

Guido Valesini (G)

Rheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico, 155, 00161 Rome, Italy.

Fabrizio Conti (F)

Rheumatology Unit, Department of Clinical Internal, Anesthesiological and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico, 155, 00161 Rome, Italy.

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Classifications MeSH