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F cγ receptors in N orwegian multiple sclerosis patients and healthy controls
Author(s) -
Gavasso S.,
Torkildsen Ø.,
Marøy T. H.,
Ulvestad E.,
Myhr K.M.,
Vedeler C. A.
Publication year - 2012
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/ane.12026
Subject(s) - multiple sclerosis , immunology , receptor , immune system , medicine , genotype , fc receptor , biology , gene , genetics
Background Multiple sclerosis ( MS ) is an immune‐mediated disease of the central nervous system in genetically susceptible persons. Fcγ receptors ( F cγ R ) are involved in autoimmune diseases. Patients and methods Sixteen Norwegian patients with relapsing–remitting MS ( RRMS ) were studied to see whether treatment with either interferon‐beta ( INF ‐β) or glatiramer acetate ( GA ) influenced the proportion of F cγ R 1a, F cγ R 2a, and F cγ R 3b positive monocytes, granulocytes, or lymphocytes or F cγ R 1a, F cγ R 2a, and F cγ R 2b mRNA levels in leukocytes. One hundred and twenty‐seven patients with RRMS and 54 N orwegian healthy blood donors were also analyzed for F cγ R 2b polymorphisms. Results Interferon‐beta or GA treatment initiated an increase in the proportion of F cγ R positive lymphocytes, but did not cause major influence of the long‐term proportion of F cγ R positive leukocytes or their F cγ R mRNA levels. No significant differences were observed between RRMS patients and healthy controls for the genotype and allele frequencies of F cγ R 2b polymorphisms. Discussion INF ‐β or GA treatment probably has no major role in the regulation of F cγ R s on immune cells in RRMS . Furthermore, polymorphisms of the inhibitory F cγ R 2b do not seem to influence the susceptibility for MS .