1. Division of Developmental Biology, The Children's Hospital Research Foundation and Department of Ophthalmology, University of Cincinnati, Cincinnati, Ohio 45229, USA
2. Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA
3. Department of Anatomy, National Defense Medical College, Tokorozawa 359-8513, Japan
4. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA
5. Department of Medicine and Molecular Cardiology Research Center, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
6. †Present addresses: Regeneron Pharmaceuticals, Tarrytown, New York 10591, USA (I.B.L.); University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA (T.J.C.); Department of Medicine, University of Sydney, New South Wales 2006, Australia (S.K.)
7. *These authors contributed equally to this work

Correspondence to: Richard A. Lang¹ Correspondence and requests for materials should be addressed to R.A.L. (Email: Richard.Lang@cchmc.org).

Abstract

Macrophages have a critical role in inflammatory and immune responses through their ability to recognize and engulf apoptotic cells¹. Here we show that macrophages initiate a cell-death programme in target cells by activating the canonical WNT pathway. We show in mice that macrophage WNT7b is a short-range paracrine signal required for WNT-pathway responses and programmed cell death in the vascular endothelial cells of the temporary hyaloid vessels of the developing eye. These findings indicate that macrophages can use WNT ligands to influence cell-fate decisions—including cell death—in adjacent cells, and raise the possibility that they do so in many different cellular contexts.

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