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Different mechanisms by which anti‐DNA MoAbs bind to human endothelial cells and glomerular mesangial cells
Author(s) -
CHAN T. M.,
FRAMPTON G.,
STAINES N. A.,
HOBBY P.,
PERRY G. J.,
CAMERON J. S.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb03041.x
Subject(s) - histone , dna , microbiology and biotechnology , biology , monoclonal antibody , umbilical vein , cell , immune system , mesangial cell , endothelial stem cell , antibody , immunology , cell culture , in vitro , biochemistry , genetics
SUMMARY The mechanisms by which anti‐DNA MoAbs derived from MRL‐lpr/lpr mice, bind to human umbilical vein endothelial cells (HUVEC) and glomerular mesangial cells were studied using a cellular ELISA. DNAse‐treatment of either the MoAb or HUVEC followed by reconstitution with DNA and/or histones was performed to determine whether DNA and histones mediated such binding. It was found that Mo Ab 410 bound to H U VEC and mesangial cells in the form of preformed DNA/anti‐DNA immune complex, and such binding was facilitated by histones. In contrast, MoAb 152 bound directly to cell membrane‐associated DNA, and adding DNA to MoAb 152 reduced its cellular binding. DNA binds endothelial cell surface and histones enhance the binding of both MoAb 410 and MoAb 152 to HUVEC by increasing cell membrane‐associated DNA. Finally, the degree of MoAb binding to HUVEC is critically influenced by the relative concentrations of antibody, DNA, and histones.

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