1990 Fiscal Year Final Research Report Summary
Mechanism of Protection of Cells from Damage of Autologous Complement
| Project/Area Number |
63480165
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
TAMUTA Nioboru Univ. of Tsukuba, Inst. Basic Med. Sci. Prof., 基礎医学系, 教授 (90076977)
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| Co-Investigator(Kenkyū-buntansha) |
FUJITA Teizo Univ. of Tsukuba, Inst. Basic. Sci., Associate Prof., 基礎医学系, 助教授 (20134223)
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| Project Period (FY) |
1988 – 1990
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| Keywords | Complement Regulatory Protein / C3 Convertase / DAF / C4NeF / C3NeF / C8 / C9 / Homologous Restriction Factor |
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| Research Abstract |
We showed in the study ; (1) decay- accelerating factor (DAF) acts as a regulatory protein by dissociating C2a or Bb from classical and alternative C3 convertases, (2) DAF on the nucleated cells exhibits the same molecular weight and activity as DAF on red cells, (3) incorporation of DAF into red cells from paroxysmal nocturnal hemoglobinuria prolongs life-span of the cells, (4) DAF functions to inhibit the assembly of C3 convertases even in the presence of C4 or C3 nephritic factor which is autoantibody against classical or alternative C3 convertase to stabilize the convertase.
Concerning a regulatory protein affecting on the late-acting components of the complement we found ; (1) it protects neuraminidase-treated human red cells from hemolysis by human complement via alternative pathway, (2) its molecular weight is 20 kDa, (3) incorpo-ration of the purified factor into guinea pig red cells renders the cells resistant to human complement attack by both classical and alternative pathways, (4) it interferes with the action of human C8 and C9, but not with that of rabbit C8 and C9. These results indicate that the factor is a homologous restriction factor.
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