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Identification of human CD93 as the phagocytic C1q receptor (C1qRp) by expression cloning
Peter Steinberger1, Andreas Szekeres, Stefan Wille
1Institute of Immunology, University of Vienna, A-1090 Vienna, Austria. peter.steinberger@univie.ac.at
Insights
The CD93 protein, also known as C1q receptor (C1qRp), is identified on myeloid cells. This study reveals CD93 enhances C1q binding and is expressed on immature dendritic cells, but not mature ones.
Area of Science:
- Immunology
- Cell Biology
- Glycoprotein Research
Background:
- CD93 is an O-sialoglycoprotein selectively expressed on myeloid lineage cells within the hematopoietic system.
- The primary structure and function of CD93 were previously unknown.
- CD93 is identical to the C1q receptor (C1qRp) found on human phagocytes, which enhances phagocytosis.
Purpose of the Study:
- To elucidate the primary structure and function of CD93.
- To identify the molecular identity of CD93.
- To investigate the role of CD93/C1qRp in immune cell function, particularly phagocytosis and dendritic cell maturation.
Main Methods:
- Retroviral-expression cloning was employed to isolate the CD93 cDNA.
- Sequence analysis was performed to determine the protein's identity.
- Expression studies were conducted on CD93 transductants, control cells, and dendritic cells at different maturation stages.
Main Results:
- Sequence analysis confirmed CD93 is identical to C1q receptor (C1qRp).
- Cells expressing CD93 demonstrated an enhanced capacity to bind C1q.
- Immature dendritic cells (DC) express CD93/C1qRp, while mature DC exhibit weak-to-negative expression.
Conclusions:
- CD93 functions as a receptor for C1q, enhancing C1q binding.
- The expression pattern of CD93/C1qRp on dendritic cells suggests a role in regulating antigen uptake and phagocytosis during DC maturation.
- CD93 is a key molecule involved in myeloid cell function and immune responses.
Abstract:
CD93 is a approximately 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.