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Original Article

Debra Gershov^a, SunJung Kim^a, Nathan Brot^a, and Keith B. Elkon^a

^a Hospital for Special Surgery, Weill Medical College of Cornell University, New York, New York 10021
Hospital for Special Surgery, 535 East 70th St., New York, NY 10021.212-774-2337212-606-1074

C-reactive protein (CRP) is a serum protein that is massively induced as part of the innate immune response to infection and tissue injury. As CRP has been detected in damaged tissues and is known to activate complement, we assessed whether apoptotic lymphocytes bound CRP and determined the effect of binding on innate immunity. CRP bound to apoptotic cells in a Ca²⁺-dependent manner and augmented the classical pathway of complement activation but protected the cells from assembly of the terminal complement components. Furthermore, CRP enhanced opsonization and phagocytosis of apoptotic cells by macrophages associated with the expression of the antiinflammatory cytokine transforming growth factor β. The antiinflammatory effects of CRP required C1q and factor H and were not effective once cells had become necrotic. These observations demonstrate that CRP and the classical complement components act in concert to promote noninflammatory clearance of apoptotic cells and may help to explain how deficiencies of the classical pathway and certain pentraxins lead to impaired handling of apoptotic cells and increased necrosis with the likelihood of immune response to self.

Key Words: apoptosis • C-reactive protein • complement • macrophages • autoimmunity

Abbreviations used in this paper: C1qd, C1q-deficient; CRP, C-reactive protein; FH, factor H; HIS, heat-inactivated sera; MAC, membrane attack complex; NHS, normal human sera; PI, propidium iodide; SAP, serum amyloid P component; SLE, systemic lupus erythematosus; snRNPs, small nuclear ribonucleoproteins.

© 2000 The Rockefeller University Press

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