Immune Complexes Bind Preferentially to FcγRIIA (CD32) on Apoptotic Neutrophils, Leading to Augmented Phagocytosis by Macrophages and Release of Proinflammatory Cytokines | Zendy

Simon P. Hart | Zendy; Karen M. Alexander | Zendy; Ian Dransfield | Zendy

Open Access

Immune Complexes Bind Preferentially to FcγRIIA (CD32) on Apoptotic Neutrophils, Leading to Augmented Phagocytosis by Macrophages and Release of Proinflammatory Cytokines

Author(s) -

Simon P. Hart,

Karen M. Alexander,

Ian Dransfield

Publication year - 2004

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.172.3.1882

Subject(s) - proinflammatory cytokine , phagocytosis , immune system , inflammation , microbiology and biotechnology , opsonin , cytokine , apoptosis , biology , immunology , tumor necrosis factor alpha , chemistry , biochemistry

Many human inflammatory diseases are associated with tissue deposition of immune complexes and influx of neutrophils. We show that immune complexes bind preferentially to apoptotic neutrophils via FcgammaRIIA (CD32) and that increased binding is associated with clustering of immune complexes on the plasma membrane of the apoptotic cell. Phagocytosis of immune complex-opsonized apoptotic neutrophils by human macrophages was substantially enhanced (4.4-fold increase compared with control apoptotic neutrophils) and stimulated macrophages to release the proinflammatory cytokines TNF-alpha and IL-6. Immune complexes may perturb the normal pathways for clearance of apoptotic neutrophils by augmenting their clearance at the price of proinflammatory cytokine release. This represents a novel mechanism by which immune complexes may modulate the resolution of inflammation.

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