| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1989: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1988: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
|---|
| Research Abstract |
Erythrocytes are hemolyzed with hetrologous complement, but not with homologous one; this evidence is called homologous restriction of complement. It has been suggested that an unidentified membrane factor is responsible for the restriction.
I tried to identify the factor. DAF, decay-accerelating factor of C3,C5-convertase, seemed to be the first candidate at the starting stage of this project, because DAF regulates the complement activation on erythrocytes. DAF was isolated from rabbit erythrocytes by an improved method applied. Both of rabbit and human DAFs showed only a weak homologous restriction. Thus, I concluded that DAF is not a major factor responsible for the restriction.
HRF, an inhibitor of membrane attack complex(MAC)-formation on human erythrocytes reported in 1986, was chosen for the second candidate. HRF, however, could not be isolated by the method described in the original paper, because the assay method was unreliable. I developed a new reliable method for detecting the inhibitor of MAC-formation, and isolated a new factor of a molecular weight 18Kd, designated MACIF. MACIF showed a potent inhibitory activity to human complement, but not to guinea pig one indicating a likely candidate responsible for the restriction. I succeeded in cDNA cloning of MACIF mRNA and determined the complete amino acid sequence of MACIF.
|
