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Interferon‐α2a effects on complement activation and regulation in MS patients
Author(s) -
Myhr K.M,
Sadallah S,
Mollnes T. E,
Meri S.,
Nyland H. I,
Schifferli J,
Vedeler C. A
Publication year - 2000
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 - 10.1034/j.1600-0404.2000.00013.x
Subject(s) - cd59 , complement system , complement (music) , recombinant dna , concomitant , complement membrane attack complex , placebo , immunology , receptor , complement receptor 1 , lysis , interferon , medicine , chemistry , immune system , biochemistry , phenotype , pathology , alternative medicine , complementation , gene
Objectives – To evaluate the treatment effect of recombinant interferona2a (rIFN‐α2a) on complement activation and regulation in MSpatients. Material and methods – Plasma levels of the complement activation products C3bc and terminal complement complex (TCC) and serum levels of the complement regulatory proteins, complement receptor 1, CR1 (CD35) and the membrane inhibitor of reactive lysis, protectin (CD59), were determined by enzyme‐linked immunosorbent assay (ELISA) in MS patients treated with IFN‐α2a (14 patients) or placebo (7 patients). Results – The level of soluble CD35 decreased while the level of TCC and to a lesser degree C3bc increased in the IFN‐α2a treated patients during the initial part of the treatment. There was also a concomitant reduction of leukocytes in the same patients. Conclusions – The results indicate that complement is activated during the initial phase of rIFN‐α2a treatment. This could partly be due to a concomitant reduction in soluble CD35