J Leukoc Biol 2001 Nov;70(5):745-8
Van Weyenbergh J, Wietzerbin J, Rouillard D, Barral-Netto M, Liblau R.
U365 INSERM, Section de Recherche, Institut Curie. U546 INSERM, Hopital La Pitie-Salpetriere, Paris, France. Goncalo Moniz Research Center, Oswaldo Cruz Foundation, Salvador-Bahia, Brazil.
Although interferon (IFN)-beta has shown a significant clinical benefit in multiple sclerosis (MS), its mechanism of action remains unclear.
We found that IFN-beta 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-beta 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-beta does
not deliver a death signal to monocytes but rather primes for subsequent
macrophage apoptosis upon activation or differentiation.
PMID: 11698494 [PubMed - in process]