Release of endogenous C3b inactivator from lymphocytes in response to triggering membrane receptors for beta 1H globulin.
Open Access
- 1 December 1980
- journal article
- research article
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 152 (6), 1625-1644
- https://doi.org/10.1084/jem.152.6.1625
Abstract
Human bone marrow-derived lymphocytes and cells from B lymphoblastoid lines were shown to have specific membrane receptors for beta 1H globin. Lymphocytes responded to the presence of beta 1H by releasing endogenously-synthesized C3b-inactivator. Very little spontaneous release of C3b-inactivator occurred in the absence of beta 1H. beta 1H-treated lymphocytes that either lacked complement receptor type one (CR1, the C4b-C3b receptor) or had their CR1 blocked with Fab9-anti-CR1 formed rosettes with C3b-coated sheep erythrocytes (EC3b) by adherence to complement receptor type two (CR2, the C3d-C3bi receptor). The mechanism of the beta 1H-induced EC3b rosette formation was shown to involve the release of lymphocyte C3b-inactivator that cleaved bound C3b into C3bi forming EC3bi. This lymphocytes-generated EC3bi then bound to CR2, forming rosettes. beta 1H-induced EC3b rosettes were completely inhibited by the presence of either anti-C3b-inactivator, F(ab9)2-anti-CR2, Fab-anti-C3c, or Fab-anti-C3d, but were unaffected by the presence of fluid-phase concentrations of beta 1H up to 5.5 mg/ml or Fab9-anti-CR1. Analysis by sodium dodecyl sulfate polyacrylamide gel electrophoresis and fluorography demonstrated that cell-free supernates of beta 1H-treated lymphocytes cleaved 3H-labeled C3b on EC3b into C3bi. Inhibition studies with chelating agents and sodium azide suggested that the release of C3b inactivator might involve a calcium and energy-dependent transport of this enzyme across the membranes of beta 1H-triggered cells. Because plasma beta 1H and C3b-inactivator are known to have important functions in the distinction of alternative pathway-activating substances from normal tissue, it is possible that this beta 1H receptor-C3b-inactivatory releasing system in lymphocytes may have an analogous function.Keywords
This publication has 32 references indexed in Scilit:
- Biosynthesis of the complement components and the regulatory proteins of the alternative complement pathway by human peripheral blood monocytes.The Journal of Experimental Medicine, 1980
- Surface markers of complement receptor lymphocytes.JCI Insight, 1978
- Human complement C3b inactivator: isolation, characterization, and demonstration of an absolute requirement for the serum protein beta1H for cleavage of C3b and C4b in solution.The Journal of Experimental Medicine, 1977
- Purification and structural analysis of the fourth component of human complementBiochemistry, 1977
- Specificity of human lymphocyte complement receptors.The Journal of Experimental Medicine, 1975
- ROLE OF COMPLEMENT IN INDUCTION OF ANTIBODY PRODUCTION IN VIVOThe Journal of Experimental Medicine, 1974
- Binding of univalent antibody fragments to a distinct antigenic determinant of staphylococcal nucleaseBiochemistry, 1974
- Protein iodination with solid state lactoperoxidaseBiochemistry, 1974
- COMPLEMENT-DEPENDENT B-CELL ACTIVATION BY COBRA VENOM FACTOR AND OTHER MITOGENS?The Journal of Experimental Medicine, 1974
- Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4Nature, 1970