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Blood, 15 May 2002, Vol. 99, No. 10, pp. 3500-3504
PLENARY PAPER
Lethal autoimmune hemolytic anemia in
CD47-deficient nonobese diabetic
(NOD) mice
Per-Arne Oldenborg,
Hattie D. Gresham,
Yongmei Chen,
Shozo Izui, and
Frederik P. Lindberg
From the Department of Integrative Medical Biology,
Section for Histology and Cell Biology, Umeå University, Umeå,
Sweden; Division of Infectious Diseases,
Department of Medicine and Department of Molecular Microbiology and
Pathogenesis, Washington University School of Medicine, St Louis, MO;
The Research Service, Albuquerque VA Medical Center and
Departments of Molecular Genetics and Microbiology, University of New
Mexico, Albuquerque; and Department of Pathology, University of
Geneva, Geneva, Switzerland.
The glycoprotein CD47 (integrin-associated protein, IAP) is present
on the surface of virtually all cells, including red blood cells
(RBCs). CD47 acts like a marker of self by ligating the macrophage
inhibitory receptor signal regulatory protein  (SIRP). In this
manner mild reactivity of wild-type RBCs with macrophage phagocytic receptors is tolerated, whereas otherwise identical CD47-deficient RBCs are rapidly eliminated. We show here that virtually
all CD47-deficient nonobese diabetic (NOD) mice spontaneously develop
severe lethal autoimmune hemolytic anemia (AIHA) at 180 to 280 days of
age, whereas none of the control CD47+ NOD mice develop
lethal AIHA at least during the first year of life. This phenotype is
at least partially due to a markedly increased rate of elimination of
opsonized CD47 / compared to CD47+ RBCs.
Similarly, CD47/C57BL/6 mice were much more sensitive
than their wild-type counterparts to experimental passive AIHA induced
by anti-RBC monoclonal antibodies. Thus, CD47-SIRP signaling can
have a profound influence on the severity of AIHA, making manipulation
of this signaling pathway a theoretically appealing avenue in the
treatment of the disease.
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