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Human Brain Endothelial Cells and Astrocytes Produce IL‐1β but not IL‐10
Author(s) -
CORSINI E.,
DUFOUR A.,
CIUSANI E.,
GELATI M.,
FRIGERIO S.,
GRITTI A.,
CAJOLA L.,
MANCARDI G. L.,
MASSA G.,
SALMAGGI A.
Publication year - 1996
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1996.d01-343.x
Subject(s) - umbilical vein , peripheral blood mononuclear cell , tumor necrosis factor alpha , astrocyte , immune system , stimulation , biology , endothelial stem cell , interleukin , messenger rna , microglia , cytokine , immunology , beta 2 microglobulin , microbiology and biotechnology , in vitro , central nervous system , endocrinology , inflammation , biochemistry , gene
The ability of human brain endothelial cells to produce mRNA for interleukin‐10, and release IL‐10 in culture supernatants after in vitro stimulation with LPS, TNF‐α and γ‐IFN was assessed and compared to that of astrocytes, peripheral blood mononuclear cells and human umbilical vein endothelial cells. IL‐1β and β 2 ‐microglobulin release were also analysed. IL‐10 and TNF‐α mRNA presence was investigated in normal brain as well as in three plaques from two multiple sclerosis patients. While increased IL‐1β and β 2 ‐microglobulin release in the supernatants of stimulated cells could be detected in all the studied cell lineages, IL‐10 mRNA and protein release was only seen in LPS‐stimulated PBMNCs. Similarly, mRNA for IL‐10 was not detected in CNS tissues, while TNF‐α was present in all plaques. The lack of production of significant amounts of IL‐10 by astrocytes and human brain endothelial cells suggests that these cells may not be the primary source of in vivo IL‐10‐mediated down‐regulation of immune reactions within the central nervous system.