IFNbeta-1b alters the composition of circulating B cell subsets, and leads to changes in the B cell cytokine secretion profile in patients with relapsing-remitting multiple sclerosis. (116.9)
| Autor: | Daniel Mielcarz, Alan Bergeron, John DeLong, Kathleen Smith, Alexandra Heyn, Karen Mack, Mary Ann Conrad, Brant Oliver, Lloyd Kasper, Jacqueline Channon |
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| Rok vydání: | 2012 |
| Předmět: | |
| Zdroj: | The Journal of Immunology. 188:116.9-116.9 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.188.supp.116.9 |
| Popis: | Recent studies provide strong evidence for a role for B cells in the pathology of RRMS. In order to explore the effect of IFNbeta-1b treatment on B cell phenotype and function in RRMS patients, blood was drawn from 10 RRMS patients before treatment and again 2 and 6 months after daily injections of IFNbeta-1b. Cryopreserved PBMCs were thawed and stained with panels of antibodies against B cell surface antigens. At baseline, RRMS patients have increased frequencies of naïve CD19+CD20+ B cells and decreased frequencies of memory B cells when compared with age-matched healthy controls. CpG-stimulated PBMCs from patients treated with IFNbeta-1b show an increase in IL-10 production and a decrease in IL-6 production by naïve, memory and B1 cells (a recently-described subset of autoantibody producing cells that are CD20+CD27+CD43+). These changes in cytokine production are indicative of a change from a pro- to an anti-inflammatory phenotype. In addition, this treatment alters the composition of circulating B cell subsets, leading to an increase after six months in circulating naïve B cells and a decrease in both memory and B1 cells, both cell types of which are potentially pathogenic in RRMS. Although the number of subjects in this study was limited, these findings suggest that alterations in B cell phenotype and function may be a mechanism by which IFNbeta-1b reduces disease activity. |
| Databáze: | OpenAIRE |
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