COMPLEMENT REGULATORY PROTEIN EXPRESSION BY A HUMAN OLIGODENDROCYTE CELL-LINE - CYTOKINE REGULATION AND COMPARISON WITH ASTROCYTES

Citation
P. Gasque et Bp. Morgan, COMPLEMENT REGULATORY PROTEIN EXPRESSION BY A HUMAN OLIGODENDROCYTE CELL-LINE - CYTOKINE REGULATION AND COMPARISON WITH ASTROCYTES, Immunology, 89(3), 1996, pp. 338-347
Citations number
38
Categorie Soggetti
Immunology
Journal title
ISSN journal
00192805
Volume
89
Issue
3
Year of publication
1996
Pages
338 - 347
Database
ISI
SICI code
0019-2805(1996)89:3<338:CRPEBA>2.0.ZU;2-2
Abstract
Rat oligodendrocytes spontaneously activate complement (C) and lack th e C inhibitor CD59. As a consequence, rat oligodendrocytes are suscept ible to lysis by autologous C in vitro. Expression of C inhibitors on human oligodendrocytes in vitro and other human glia has yet to be wel l characterized. We have previously shown expression at the mRNA level of the membrane inhibitors CD59, decay-accelerating factor (DAF; CD55 ) and membrane cofactor protein (MCP; CD46) in human astrocytes. We he re examine the expression of membrane and secreted C inhibitors by the oligodendrocyte cell line, HOG. HOG cells abundantly expressed CD59, assessed at protein and mRNA level, and expressed DAF and MCP, albeit at a lower level. Expression of all three inhibitors was enhanced by i ncubation with interferon-gamma or with phorbol ester (PMA). Complemen t receptor type 1 (CR1; CD35) was neither expressed constitutively nor induced by cytokines. HOG also constitutively secreted C1-inhibitor, S-protein and clusterin. Factor H was secreted only after stimulation with cytokines. C4b binding protein was expressed at a very low level and was detected only al the mRNA level by reverse transcriptase-polym erase chain reaction (RT-PCR). For comparison, astrocyte expression of CD59, DAF, MCP and CR1 was confirmed at the mRNA and protein levels. HOG did not activate C spontaneously, as judged by the lack of deposit ion of C fragments, and were not lysed by C even after inhibition of C D59 and DAF using specific monoclonal antibodies.