Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 223, Issue 1-2, Pages 135-137Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jneuroim.2010.03.015
Keywords
Multiple sclerosis; Clinically isolated syndrome; B cell; Fc receptor; Autoimmunity
Categories
Funding
- Bavarian Genome Research Network (BayGene)
- German Research Foundation [SFB643, FOR832]
- Paul Ehrlich and Ludwig Darmstaedter foundation
- Bayer-Schering
- Biogen-Idec
- Merck-Serono
- Teva
- Sanofi-Aventis
- Novartis
- Dana Foundation
- Cancer Research Institute
- Swiss National Science Foundation
- Gemeinnutzige Hertie Stiftung
- Swiss Multiple Sclerosis Society
- Baxter
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Expression of the inhibitory Fc gamma receptor IIB (Fc gamma RIIB) has emerged as a late checkpoint during peripheral B cell development which prevents autoreactive memory B lymphocytes from becoming long-lived plasma cells. Decreased expression of Fc gamma RIIB or non-functional Fc gamma RIIB variants are associated with the development of autoimmune tissue inflammation. We determined the expression profile of Fc gamma RIIB in peripheral blood cells in treatment-naive patients with early MS. Twenty-five patients with clinically isolated syndrome (CIS) who converted to clinically definite MS (CDMS) and 25 demographically matched healthy donors were included in the study. Frequencies of peripheral blood monocytes and B cell subsets as well as Fc gamma RIIB expression profile was determined by flow cytometry. Fc gamma RIIB expression levels were higher in B cells compared to monocytes (p<0.0001) and higher in memory B cells compared to their naive counterparts (p<0.0001). However, Fc gamma RIIB expression in naive and memory B cells as well as monocytes was unchanged in patients with early MS at onset of symptoms as well as after conversion to CDMS compared to controls. No significant correlations were found between Fc gamma RIIB expression levels and brain MRI-derived metrics or EDSS progression during follow-up. These data indicate that Fc gamma RIIB expression, a critical late B cell differentiation checkpoint preventing the occurrence of autoreactive long-lived plasma cells, is not impaired in treatment-naive patients with MS, at least in the early phases of the disease. (C) 2010 Elsevier B.V. All rights reserved.
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