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Blood, 1 January 2006, Vol. 107, No. 1, pp. 341-348.
Prepublished online as a Blood First Edition Paper on September 1, 2005; DOI 10.1182/blood-2005-05-1896.
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RED CELLS
SHPS-1 promotes the survival of circulating erythrocytes through inhibition of phagocytosis by splenic macrophages
Tomomi Ishikawa-Sekigami,
Yoriaki Kaneko,
Hideki Okazawa,
Takeshi Tomizawa,
Jun Okajo,
Yasuyuki Saito,
Chie Okuzawa,
Minako Sugawara-Yokoo,
Uichi Nishiyama,
Hiroshi Ohnishi,
Takashi Matozaki, and
Yoshihisa Nojima
From the Department of Medicine and Clinical Science, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan; Laboratory of Biosignal Sciences, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan; and Pharmaceutical Development Laboratories, Kirin Brewery Co Ltd, Takasaki, Gunma, Japan.
The lifespan of circulating red blood cells (RBCs) produced in bone marrow is determined by their elimination through phagocytosis by splenic macrophages. The mechanism by which RBC elimination is regulated has remained unclear, however. The surface glycoprotein SHPS-1, a member of the immunoglobulin superfamily, is abundant in macrophages. We have now examined the regulation of RBC turnover with the use of mice that express a mutant form of SHPS-1 lacking most of its cytoplasmic region. The mutant mice manifested mild anemia as well as splenomegaly characterized by expansion of the red pulp. The numbers of erythroid precursor cells in the spleen and of circulating reticulocytes were also increased in the mutant mice. In contrast, the half-life of circulating RBCs was reduced in these animals, and the rate of clearance of injected opsonized RBCs from the peripheral circulation was increased in association with their incorporation into splenic macrophages. Phagocytosis of opsonized RBCs by splenic macrophages from mutant mice in vitro was also increased compared with that observed with wild-type macrophages. These results suggest that SHPS-1 negatively regulates the phagocytosis of RBCs by splenic macrophages, thereby determining both the lifespan of individual RBCs and the number of circulating erythrocytes.
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