title: Interferon-beta treatment alters peripheral blood monocytes chemokine production in MS patients.
abstract: Chemokines direct the recruitment of leukocytes to inflammatory sites and may also participate in the regulation of cytokine production by naive T helper cells. Chemokine production by blood monocytes was investigated by intracytoplasmic staining in interferon-beta (IFN-beta)-treated multiple sclerosis (MS) patients, untreated MS patients, and healthy controls. Under unstimulated conditions, no differences in the production of interleukin-8 (IL-8), IFN-inducible protein 10 (IP-10), monokine induced by interferon-gamma (Mig), monocyte chemoattractant protein-1 (MCP-1), and monocyte chemoattractant protein-3 (MCP-3) were seen between untreated MS patients and controls. Chemokine production by monocytes following T cell activation was decreased in MS patients taking IFN-beta compared to controls and untreated MS patients. Unlike other chemokines, macrophage inflammatory protein-1alpha (MIP-1alpha) production by monocytes was significantly decreased in untreated MS patients compared to controls, and IFN-beta treatment increased MIP-1alpha expression to the level seen in controls. In vitro addition of IFN-beta1b to peripheral blood mononuclear cells (PBMC) cultures tended to decrease the production of IL-8, IP-10, Mig, MCP-1, and MCP-3, but not of MIP-1alpha. These findings suggest that IFN-beta treatment may have a differential affect on chemokine production by monocytes. Longitudinal studies must be done to confirm these observations.
authors.affiliation: Center for Neurologic Diseases, Brigham and Women's Hospital, 77 Avenue Louis Pasteur, HIM 714, Boston, MA 02115, USA.
authors.forename: Manuel
authors.initials: M
authors.lastname: Comabella
authors.forename: Jaime
authors.initials: J
authors.lastname: Imitola
authors.forename: Howard L
authors.initials: HL
authors.lastname: Weiner
authors.forename: Samia J
authors.initials: SJ
authors.lastname: Khoury
mesh_terms: D000276:Adjuvants, Immunologic / Q000008:administration & dosage*; D000328:Adult; D023201:CD40 Ligand / Q000276:immunology; D018932:Chemokine CCL2 / Q000096:biosynthesis; D054410:Chemokine CCL7; D054357:Chemokine CXCL10 / Q000096:biosynthesis; D054370:Chemokine CXCL9; D019743:Chemokines, CXC / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D036341:Intercellular Signaling Peptides and Proteins; D016899:Interferon-beta / Q000008:administration & dosage*; D016753:Interleukin-10 / Q000276:immunology; D016209:Interleukin-8 / Q000096:biosynthesis; D008297:Male; D018945:Monocyte Chemoattractant Proteins / Q000096:biosynthesis; D009000:Monocytes / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D009103:Multiple Sclerosis / Q000188:drug therapy* / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D000276:Adjuvants, Immunologic; C515450:CCL7 protein, human; C080810:CXCL9 protein, human; D018932:Chemokine CCL2; D054410:Chemokine CCL7; D054357:Chemokine CXCL10; D054370:Chemokine CXCL9; D019743:Chemokines, CXC; D016207:Cytokines; D036341:Intercellular Signaling Peptides and Proteins; D016209:Interleukin-8; D018945:Monocyte Chemoattractant Proteins; D016753:Interleukin-10; D023201:CD40 Ligand; D016899:Interferon-beta