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Blood, 1 July 2005, Vol. 106, No. 1, pp. 207-215.
Prepublished online as a Blood First Edition Paper on March 22, 2005; DOI 10.1182/blood-2004-12-4943.
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IMMUNOBIOLOGY
Lack of antigen-specific tissue remodeling in mice deficient in the macrophage galactose-type calcium-type lectin 1/CD301a
Kayoko Sato,
Yasuyuki Imai,
Nobuaki Higashi,
Yosuke Kumamoto,
Thandi M. Onami,
Stephen M. Hedrick, and
Tatsuro Irimura
From the Laboratory of Cancer Biology and Molecular Immunology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Japan; the Department of Microbiology, University of Shizuoka, School of Pharmaceutical Sciences, Shizuoka, Japan; and the Molecular Biology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA.
Macrophage galactose-type C-type lectins (MGLs), which were recently named CD301, have 2 homologues in mice: MGL1 and MGL2. MGLs are expressed on macrophages and immature dendritic cells. The persistent presence of granulation tissue induced by a protein antigen was observed in wild-type mice but not in mice lacking an endogenous, macrophage-specific, galactose-type calcium-type lectin 1 (MGL1) in an air pouch model. The anti-MGL1 antibody suppressed the granulation tissue formation in wild-type mice. A large number of cells, present only in the pouch of MGL1-deficient mice, were not myeloid or lymphoid lineage cells and the number significantly declined after administration of interleukin 1 (IL-1 ) into the pouch of MGL1-deficient mice. Furthermore, granulation tissue was restored by this treatment and the cells obtained from the pouch of MGL1-deficient mice were incorporated into the granulation tissue when injected with IL-1 . Taken together, MGL1 expressed on a specific subpopulation of macrophages that secrete IL-1 was proposed to regulate specific cellular interactions crucial to granulation tissue formation.

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