Short-term treatment of relapsing remitting multiple sclerosis patients with interferon (IFN)beta 1b transiently increases the blood levels of interleukin (IL)-6, IL-10 and IFN-gamma without significantly modifying those of IL-1 beta, IL-2, IL-4 and tumour necrosis factor-alpha

Citation
F. Nicoletti et al., Short-term treatment of relapsing remitting multiple sclerosis patients with interferon (IFN)beta 1b transiently increases the blood levels of interleukin (IL)-6, IL-10 and IFN-gamma without significantly modifying those of IL-1 beta, IL-2, IL-4 and tumour necrosis factor-alpha, CYTOKINE, 12(6), 2000, pp. 682-687
Citations number
38
Categorie Soggetti
Cell & Developmental Biology
Journal title
CYTOKINE
ISSN journal
10434666 → ACNP
Volume
12
Issue
6
Year of publication
2000
Pages
682 - 687
Database
ISI
SICI code
1043-4666(200006)12:6<682:STORRM>2.0.ZU;2-3
Abstract
We have studied the impact of short-term treatment with interferon (IFN)-be ta 1b of relapsing remitting (RR) multiple sclerosis (MS) patients' blood l evels of type 1 and type 2 cytokines such as IFN-gamma, interleukin (IL)-1 beta, IL-2, IL-3, IL-6, IL-10 and tumour necrosis factor (TNF)-alpha, These cytokines were measured by solid-phase ELISA, Serum samples were obtained prior to, and 2 and 12 hours after beginning of the treatment and 48 h afte r the last of 5 s.c. injections with 8 million TU IFN-beta 1b given on alte rnate days for 10 days. The treatment was found to increase the circulating levels of IL-2, IL-6, IL-10 and IFN-gamma at some of the time points consi dered, with the effect acquiring statistical significance for IL-6, IL-10 a nd IFN-gamma, The blood levels of IL-1 beta, IL-4 and TNF-alpha remained be low the limit of sensitivity of the assays at any of the time points consid ered. If this in vivo study mirrors the impact of IFN-beta 1b on MS patient s' immune cells, these data demonstrate an activation of the immune system upon early treatment with the drug that does not lead to either type 1 or t ype 2 cytokine prevalence. (C) 2000 Academic Press.