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C4b-binding protein and factor h compensate for the loss of membrane-bound complement inhibitors to protect apoptotic cells against excessive complement attack

In English

Författare

Summary, in English

Apoptotic cells have been reported to down- regulate membrane-bound complement regulatory proteins ( m- C- Reg) and to activate complement. Nonetheless, most apoptotic cells do not undergo complement- mediated lysis. Therefore, we hypothesized that fluid phase complement inhibitors would bind to apoptotic cells and compensate functionally for the loss of m- C- Reg. We observed that m- C- Reg are down- regulated rapidly upon apoptosis but that complement activation follows only after a gap of several hours. Coinciding with, but independent from, complement activation, fluid phase complement inhibitors C4b- binding protein ( C4BP) and factorH( fH) bind to the cells. C4BP and fH do not entirely prevent complement activation but strongly limit C3 and C9 deposition. Late apoptotic cells, present in blood of healthy controls and systemic lupus erythematosus patients, are also positive for C4BP and fH. Upon culture, the percentage of late apoptotic cells increases, paralleled by increased C4BP binding. C4BP binds to dead cells mainly via phosphatidylserine, whereas fH binds via multiple interactions with CRP playing no major role for binding of C4BP or fH. In conclusion, during late apoptosis, cells acquire fluid phase complement inhibitors that compensate for the downregulation of m- C- Reg and protect against excessive complement activation and lysis.

Publiceringsår

2007

Språk

Engelska

Sidor

28540-28548

Publikation/Tidskrift/Serie

Journal of Biological Chemistry

Volym

282

Issue

39

Dokumenttyp

Artikel i tidskrift

Förlag

American Society for Biochemistry and Molecular Biology

Ämne

  • Rheumatology and Autoimmunity
  • Immunology in the medical area
  • Medicinal Chemistry

Status

Published

Forskningsgrupp

  • Clinical Chemistry, Malmö
  • Protein Chemistry, Malmö
  • Immunology

ISBN/ISSN/Övrigt

  • ISSN: 1083-351X