title: MIG--differential gene expression in mouse brain endothelial cells.
abstract: Different diseases of the CNS are associated with blood-brain barrier (BBB) damage and mononuclear cell infiltration. In order to study genes that may play a role in endothelial cell regulation in inflammatory CNS diseases, we performed differential gene expression (DGE) analysis using a mouse brain endothelial cell line. We found that interferon-gamma (IFNgamma)-induced monokine (MIG), a chemokine that plays a role in T lymphocyte and monocyte chemoattraction, is highly expressed in the presence of inflammatory cytokines. We show that MIG, produced by brain endothelial cells in vitro, is biologically active in attractingT lymphocytes and that it is possible to interfere with this mechanism of action using anti-MIG antibodies. We suggest that blocking MIG may be beneficial in CNS inflammation. We detected constitutive expression of the MIG receptor, CXCR3, on the surface of the endothelial cells and therefore hypothesize that it plays a role in maintaining the cytokine gradient at the region of CNS inflammation.
authors.affiliation: Serono Pharmaceutical Research Institute, Geneva, Switzerland.
authors.forename: Paola
authors.initials: P
authors.lastname: Ghersa
authors.forename: Maurizio
authors.initials: M
authors.lastname: Gelati
authors.forename: Jacques
authors.initials: J
authors.lastname: Colinge
authors.forename: Georg
authors.initials: G
authors.lastname: Feger
authors.forename: Christine
authors.initials: C
authors.lastname: Power
authors.forename: Paola
authors.initials: P
authors.lastname: Ghersa
authors.forename: Maurizio
authors.initials: M
authors.lastname: Gelati
authors.forename: Jacques
authors.initials: J
authors.lastname: Colinge
authors.forename: Georg
authors.initials: G
authors.lastname: Feger
authors.forename: Christine
authors.initials: C
authors.lastname: Power
authors.forename: Ruben
authors.initials: R
authors.lastname: Papoian
authors.forename: Andrea
authors.initials: A
authors.lastname: Salmaggi
mesh_terms: D000818:Animals; D001921:Brain / Q000166:cytology / Q000502:physiology*; D054370:Chemokine CXCL9; D019743:Chemokines, CXC / Q000235:genetics* / Q000502:physiology; D002634:Chemotaxis, Leukocyte / Q000502:physiology; D004338:Drug Combinations; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D015870:Gene Expression / Q000187:drug effects; D036341:Intercellular Signaling Peptides and Proteins; D007371:Interferon-gamma / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology; D007376:Interleukin-2 / Q000494:pharmacology; D051379:Mice; D020411:Oligonucleotide Array Sequence Analysis; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine / Q000378:metabolism; D014407:Tumor Cells, Cultured; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D015854:Up-Regulation
chemical_list: C080810:CXCL9 protein, human; C515187:CXCR3 protein, human; D054370:Chemokine CXCL9; D019743:Chemokines, CXC; C515188:Cxcr3 protein, mouse; D004338:Drug Combinations; D036341:Intercellular Signaling Peptides and Proteins; D007375:Interleukin-1; D007376:Interleukin-2; D054367:Receptors, CXCR3; D019707:Receptors, Chemokine; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma