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(Journal of Leukocyte Biology. 2002;71:133-140.)
© 2002 by Society for Leukocyte Biology

Identification of human CD93 as the phagocytic C1q receptor (C1qRp) by expression cloning

Peter Steinberger*, Andreas Szekeres{dagger}, Stefan Wille*, Johannes Stöckl*, Nicole Selenko*, Elisabeth Prager{dagger}, Günther Staffler{dagger}, Otto Madic*, Hannes Stockinger{dagger} and Walter Knapp*,{dagger}

* Institute of Immunology, University of Vienna, A-1090 Vienna, Austria; and
{dagger} Institute of Immunology— Vienna International Research Cooperation Center at NFI, University of Vienna, A-1235 Vienna, Austria

Correspondence: Dr. Peter Steinberger, Institute of Immunology, University of Vienna, Borschkegasse 8a, A-1090 Vienna, Austria. E-mail: peter.steinberger{at}univie.ac.at

CD93 is a ~120 kDa O-sialoglycoprotein that within the hematopoietic system is selectively expressed on cells of the myeloid lineage. So far, its primary structure and function were unknown. We used retroviral-expression cloning to isolate the CD93 cDNA. Sequence analysis revealed that CD93 is identical to a protein on human phagocytes termed C1q receptor (C1qRp). C1qRp was shown previously to mediate enhancement of phagocytosis in monocytes and was suggested to be a receptor of C1q and two other structurally related molecules. When studying CD93 transductants and control cells, we found that cells expressing CD93 have enhanced capacity to bind C1q. Furthermore, we show that immature dendritic cells (DC) express CD93/C1qRp, and mature DC, known to have reduced capacity for antigen uptake and to have lost the ability to phagocytose, show weak-to-negative CD93/C1qRp expression.

Key Words: dendritic cells • cell-surface molecules • complement • molecular biology




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