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(Journal of Leukocyte Biology. 2002;71:881-889.)
© 2002 by Society for Leukocyte Biology

Recognition and phagocytosis of apoptotic T cells by resident murine tissue macrophages require multiple signal transduction events

Bin Hu^*, Antonello Punturieri^*,, Jill Todt^*, Joanne Sonstein^*, Timothy Polak^* and Jeffrey L. Curtis^*,

^* Division of Pulmonary & Critical Care Medicine, Department of Internal Medicine, University of Michigan Health System, Ann Arbor; and
Pulmonary & Critical Care Medicine Section, Medical Service, Department of Veterans Affairs Medical Center, Ann Arbor, Michigan

Correspondence: Jeffrey L. Curtis, M.D., Pulmonary & Critical Care Medicine Section (111G), Department of Veterans Affairs Medical Center, 2215 Fuller Rd., Ann Arbor, MI 48105-2303. E-mail: jlcurtis{at}umich.edu

Macrophages (Mø) ingest apoptotic cells with unique effects on their cytokine production, but the signaling pathways involved are virtually unknown. Signal transduction in response to recognition of apoptotic thymocytes by resident murine alveolar (AMø) or peritoneal (PMø) Mø was studied by in vitro phagocytosis assay. Phagocytosis was decreased in a dose-dependent and nontoxic manner by inhibiting phosphatidylinositol 3 kinase (wortmannin and LY294002), protein tyrosine phosphorylation (herbimycin A, genistein, piceatannol, and for AMø only, PP2), and protein kinase C (staurosporine, Gö 6976, and calphostin C). Exposure of Mø to apoptotic or heat-killed thymocytes, but not to viable thymocytes, activated ERK1/2 rapidly, as detected by specific phosphorylation, but did not activate NF-B or MAP kinases p38 or JNK. Mø phagocytosis of apoptotic T cells requires tyrosine, serine/threonine, and lipid phosphorylation. Mø recognition of apoptotic T cells triggers rapid but limited MAP kinase activation.

Key Words: apoptosis • lung • protein kinases/phosphatases

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