Frequency and immunophenotype of IL10-producing regulatory B cells in optic neuritis.
clinically isolated syndrome
interleukin-10
multiple sclerosis
optic neuritis
regulatory B cells
Journal
Immunology
ISSN: 1365-2567
Titre abrégé: Immunology
Pays: England
ID NLM: 0374672
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
13
05
2018
revised:
22
10
2018
accepted:
02
11
2018
pubmed:
20
11
2018
medline:
30
8
2019
entrez:
20
11
2018
Statut:
ppublish
Résumé
Mouse models of multiple sclerosis (MS) have shown the importance of interleukin-10 (IL-10) -producing regulatory B (Breg) cells in dampening disease activity and inhibiting disease initiation and progression. In MS and other autoimmune diseases decreased frequency and functionality of Breg cells correlate with disease activity and the percentage of IL-10-producing Breg cells decreases during relapse and normalizes in remission. Optic neuritis (ON) is a common first clinical manifestation of MS and IL-10-producing Breg cells may be crucial in the transition from ON to MS, we therefore investigate the frequency and function of Breg cells in ON as a clinical model of early demyelinating disease. B cells were purified from 27 patients with ON sampled close to symptom onset (median 23 days, range 7-41 days) and 13 healthy controls. The B cells were stimulated and cultured for 48 hr with CD40 ligand and CpG before measurement of intracellular IL-10 and the surface markers CD19, CD1d, CD5, CD24, CD38 and CD27 by flow cytometry. The frequency of B-cell subsets was analysed in peripheral blood and cerebral spinal fluid (CSF) of patients. Sixty-five per cent of the IL-10-producing Breg cells co-expressed CD24 and CD38, and only 14% were CD24
Identifiants
pubmed: 30452090
doi: 10.1111/imm.13024
pmc: PMC6376272
doi:
Substances chimiques
IL10 protein, human
0
Interleukin-10
130068-27-8
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
259-269Informations de copyright
© 2018 John Wiley & Sons Ltd.
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