Complement regulatory protein expression by a human oligodendrocyte cell line: Cytokine regulation and comparison with astrocytes

被引:55
作者
Gasque, P
Morgan, BP
机构
[1] Department of Medical Biochemistry, UWCM, Tenovus Building, Cardiff, Heath Park
[2] Department of Medical Biochemistry, UWCM, Tenovus Building, Cardiff, CF4 4XX, Heath Park
基金
英国惠康基金;
关键词
D O I
10.1046/j.1365-2567.1996.d01-756.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Rat oligodendrocytes spontaneously activate complement (C) and lack the C inhibitor CD59. As a consequence, rat oligodendrocytes are susceptible to lysis by autologous C in vitro. Expression of C inhibitors on human oligodendrocytes in vitro and other human glia has yet to be well 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 here 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 incubation with interferon-gamma or with phorbol ester (PMA). Complement 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-polymerase 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 deposition of C fragments, and were not lysed by C even after inhibition of CD59 and DAF using specific monoclonal antibodies.
引用
收藏
页码:338 / 347
页数:10
相关论文
共 38 条
[1]  
CYONG JC, 1992, J EXP MED, V155, P587
[2]   THE ROLE OF COMPLEMENT IN INFLAMMATION AND PHAGOCYTOSIS [J].
FRANK, MM ;
FRIES, LF .
IMMUNOLOGY TODAY, 1991, 12 (09) :322-326
[3]  
GASQUE P, 1992, J IMMUNOL, V149, P1381
[4]  
GASQUE P, 1995, J IMMUNOL, V154, P4726
[5]  
GASQUE P, 1993, J BIOL CHEM, V268, P25068
[6]  
HARA T, 1992, CLIN EXP IMMUNOL, V89, P490
[7]   COMPLEMENT MESSENGER-RNA IN THE MAMMALIAN BRAIN - RESPONSES TO ALZHEIMERS-DISEASE AND EXPERIMENTAL BRAIN LESIONING [J].
JOHNSON, SA ;
LAMPERTETCHELLS, M ;
PASINETTI, GM ;
ROZOVSKY, I ;
FINCH, CE .
NEUROBIOLOGY OF AGING, 1992, 13 (06) :641-648
[8]  
JOHNSTONE RW, 1993, IMMUNOLOGY, V79, P341
[9]  
KASHIMA T, 1993, CANCER RES, V53, P170
[10]   UNEXPECTED EXPRESSION OF INTERMEDIATE FILAMENT PROTEIN GENES IN HUMAN OLIGODENDROGLIOMA CELL-LINES [J].
KASHIMA, T ;
VINTERS, HV ;
CAMPAGNONI, AT .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1995, 54 (01) :23-31