Functional overlap but differential expression of CSF-1 and IL-34 in their CSF-1 receptor-mediated regulation of myeloid cells (original) (raw)

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Department of Developmental and Molecular Biology, Albert Einstein College of Medicine

, Bronx, New York,

USA

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Department of Developmental and Molecular Biology, Albert Einstein College of Medicine

, Bronx, New York,

USA

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Department of Developmental and Molecular Biology, Albert Einstein College of Medicine

, Bronx, New York,

USA

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,

Department of Developmental and Molecular Biology, Albert Einstein College of Medicine

, Bronx, New York,

USA

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Department of Developmental and Molecular Biology, Albert Einstein College of Medicine

, Bronx, New York,

USA

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Five Prime Therapeutics, Inc., San Francisco

, California,

USA

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Five Prime Therapeutics, Inc., San Francisco

, California,

USA

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Five Prime Therapeutics, Inc., San Francisco

, California,

USA

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Department of Developmental and Molecular Biology, Albert Einstein College of Medicine

, Bronx, New York,

USA

Correspondence: Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA. E-mail: richard.stanley@einstein.yu.edu

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Received:

24 December 2009

Revision received:

05 May 2010

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Suwen Wei, Sayan Nandi, Violeta Chitu, Yee-Guide Yeung, Wenfeng Yu, Minmei Huang, Lewis T Williams, Haishan Lin, E Richard Stanley, Functional overlap but differential expression of CSF-1 and IL-34 in their CSF-1 receptor-mediated regulation of myeloid cells, Journal of Leukocyte Biology, Volume 88, Issue 3, September 2010, Pages 495–505, https://doi.org/10.1189/jlb.1209822
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Abstract

CSF-1 and the novel CSF-1 receptor ligand, IL-34, possess similar CSF-1R-mediated activities, but differ in their spatio-temporal expression, permitting complementary CSF-1 receptor activation in vivo.

CSF-1 is broadly expressed and regulates macrophage and osteoclast development. The action and expression of IL-34, a novel CSF-1R ligand, were investigated in the mouse. As expected, huIL-34 stimulated macrophage proliferation via the huCSF-1R, equivalently to huCSF-1, but was much less active at stimulating mouse macrophage proliferation than huCSF-1. Like muCSF-1, muIL-34 and a muIL-34 isoform lacking Q81 stimulated mouse macrophage proliferation, CSF-1R tyrosine phosphorylation, and signaling and synergized with other cytokines to generate macrophages and osteoclasts from cultured progenitors. However, they respectively possessed twofold and fivefold lower affinities for the CSF-1R and correspondingly, lower activities than muCSF-1. Furthermore, muIL-34, when transgenically expressed in a CSF-1-dependent manner in vivo, rescued the bone, osteoclast, tissue macrophage, and fertility defects of Csf1_op_/op mice, suggesting similar regulation of CSF-1R-expressing cells by IL-34 and CSF-1. Whole-mount IL34 in situ hybridization and CSF-1 reporter expression revealed that IL34 mRNA was strongly expressed in the embryonic brain at E11.5, prior to the expression of Csf1 mRNA. QRT-PCR revealed that compared with Csf1 mRNA, IL34 mRNA levels were lower in pregnant uterus and in cultured osteoblasts, higher in most regions of the brain and heart, and not compensatorily increased in Csf1 op/op mouse tissues. Thus, the different spatiotemporal expression of IL-34 and CSF-1 allows for complementary activation of the CSF-1R in developing and adult tissues.

© 2010 Society for Leukocyte Biology

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