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Treatment of multiple sclerosis patients with interferon‐β primes monocyte‐derived macrophages for apoptotic cell death
Author(s) -
Van Weyenbergh Johan,
Wietzerbin Juana,
Rouillard Dany,
BarralNetto Manoel,
Liblau Roland
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.70.5.745
Subject(s) - apoptosis , biology , annexin , monocyte , programmed cell death , immunology , interferon , multiple sclerosis , in vivo , macrophage , dna fragmentation , annexin a5 , cancer research , in vitro , microbiology and biotechnology , biochemistry
Although interferon (IFN)‐β has shown a significant clinical benefit in multiple sclerosis (MS), its mechanism of action remains unclear. We found that IFN‐β treatment of patients with MS resulted in a significant increase in apoptotic cell death (measured by annexin V staining and nuclear fragmentation) of monocyte‐derived macrophages, as compared with cells derived from patients before treatment. Stimulation of the cells with IFN‐β in vitro resulted in an even further increase of annexin V binding, as well as increased Fas (CD 95, APO‐1) expression. However, no increased Fas expression, apoptotic monocytes, or monocytopenia were observed upon in vivo treatment. This indicates that IFN‐β does not deliver a death signal to monocytes but rather primes for subsequent macrophage apoptosis upon activation or differentiation.