Decay accelerating factor regulates complement activation on glomerular epithelial cells

R. J. Quigg, A. Nicholson-Weller, A. V. Cybulsky, John Badalamenti, D. J. Salant

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

Epithelial cells of the glomerular capillary are the site of C5b-9 mediated injury in rat membranous nephropathy. We investigated the regulation of C activation by cultured glomerular epithelial cells (GEC). Rat and human GEC were more resistant to C injury by homologous C than heterologous C. In human GEC homologous C cytotoxicity was enhanced by antiserum to decay accelerating factor (DAF) indicating that homologous C activation was, at least in part, restricted by membrane DAF. Anti-DAF immunoprecipitated a 67-kDa protein from human glomeruli. In rat GEC, pronase and phosphatidylinositol-specific phospholipase C (which are known to inactivate human DAF) enhanced cytotoxicity by homologous C. Thus, DAF is present on human GEC in culture and in human kidney glomeruli, and a DAF-like protein is present on cultured rat GEC. These proteins regulate C activation in vitro and may play a role in controlling C activation on GEC in vivo.

Original languageEnglish (US)
Pages (from-to)877-882
Number of pages6
JournalJournal of Immunology
Volume142
Issue number3
StatePublished - 1989
Externally publishedYes

Fingerprint

CD55 Antigens
Complement Activation
Epithelial Cells
Kidney Glomerulus
Phosphoinositide Phospholipase C
Complement Membrane Attack Complex
Membranous Glomerulonephritis
Pronase
Wounds and Injuries
Protein C
Immune Sera
Proteins
Cell Culture Techniques
Membranes

ASJC Scopus subject areas

  • Immunology

Cite this

Quigg, R. J., Nicholson-Weller, A., Cybulsky, A. V., Badalamenti, J., & Salant, D. J. (1989). Decay accelerating factor regulates complement activation on glomerular epithelial cells. Journal of Immunology, 142(3), 877-882.

Decay accelerating factor regulates complement activation on glomerular epithelial cells. / Quigg, R. J.; Nicholson-Weller, A.; Cybulsky, A. V.; Badalamenti, John; Salant, D. J.

In: Journal of Immunology, Vol. 142, No. 3, 1989, p. 877-882.

Research output: Contribution to journalArticle

Quigg, RJ, Nicholson-Weller, A, Cybulsky, AV, Badalamenti, J & Salant, DJ 1989, 'Decay accelerating factor regulates complement activation on glomerular epithelial cells', Journal of Immunology, vol. 142, no. 3, pp. 877-882.
Quigg, R. J. ; Nicholson-Weller, A. ; Cybulsky, A. V. ; Badalamenti, John ; Salant, D. J. / Decay accelerating factor regulates complement activation on glomerular epithelial cells. In: Journal of Immunology. 1989 ; Vol. 142, No. 3. pp. 877-882.
@article{6c4ac91dec08456d82682edbe57ebcac,
title = "Decay accelerating factor regulates complement activation on glomerular epithelial cells",
abstract = "Epithelial cells of the glomerular capillary are the site of C5b-9 mediated injury in rat membranous nephropathy. We investigated the regulation of C activation by cultured glomerular epithelial cells (GEC). Rat and human GEC were more resistant to C injury by homologous C than heterologous C. In human GEC homologous C cytotoxicity was enhanced by antiserum to decay accelerating factor (DAF) indicating that homologous C activation was, at least in part, restricted by membrane DAF. Anti-DAF immunoprecipitated a 67-kDa protein from human glomeruli. In rat GEC, pronase and phosphatidylinositol-specific phospholipase C (which are known to inactivate human DAF) enhanced cytotoxicity by homologous C. Thus, DAF is present on human GEC in culture and in human kidney glomeruli, and a DAF-like protein is present on cultured rat GEC. These proteins regulate C activation in vitro and may play a role in controlling C activation on GEC in vivo.",
author = "Quigg, {R. J.} and A. Nicholson-Weller and Cybulsky, {A. V.} and John Badalamenti and Salant, {D. J.}",
year = "1989",
language = "English (US)",
volume = "142",
pages = "877--882",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "3",

}

TY - JOUR

T1 - Decay accelerating factor regulates complement activation on glomerular epithelial cells

AU - Quigg, R. J.

AU - Nicholson-Weller, A.

AU - Cybulsky, A. V.

AU - Badalamenti, John

AU - Salant, D. J.

PY - 1989

Y1 - 1989

N2 - Epithelial cells of the glomerular capillary are the site of C5b-9 mediated injury in rat membranous nephropathy. We investigated the regulation of C activation by cultured glomerular epithelial cells (GEC). Rat and human GEC were more resistant to C injury by homologous C than heterologous C. In human GEC homologous C cytotoxicity was enhanced by antiserum to decay accelerating factor (DAF) indicating that homologous C activation was, at least in part, restricted by membrane DAF. Anti-DAF immunoprecipitated a 67-kDa protein from human glomeruli. In rat GEC, pronase and phosphatidylinositol-specific phospholipase C (which are known to inactivate human DAF) enhanced cytotoxicity by homologous C. Thus, DAF is present on human GEC in culture and in human kidney glomeruli, and a DAF-like protein is present on cultured rat GEC. These proteins regulate C activation in vitro and may play a role in controlling C activation on GEC in vivo.

AB - Epithelial cells of the glomerular capillary are the site of C5b-9 mediated injury in rat membranous nephropathy. We investigated the regulation of C activation by cultured glomerular epithelial cells (GEC). Rat and human GEC were more resistant to C injury by homologous C than heterologous C. In human GEC homologous C cytotoxicity was enhanced by antiserum to decay accelerating factor (DAF) indicating that homologous C activation was, at least in part, restricted by membrane DAF. Anti-DAF immunoprecipitated a 67-kDa protein from human glomeruli. In rat GEC, pronase and phosphatidylinositol-specific phospholipase C (which are known to inactivate human DAF) enhanced cytotoxicity by homologous C. Thus, DAF is present on human GEC in culture and in human kidney glomeruli, and a DAF-like protein is present on cultured rat GEC. These proteins regulate C activation in vitro and may play a role in controlling C activation on GEC in vivo.

UR - http://www.scopus.com/inward/record.url?scp=0024566684&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024566684&partnerID=8YFLogxK

M3 - Article

VL - 142

SP - 877

EP - 882

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 3

ER -