C1QR(P), THE C1Q RECEPTOR THAT ENHANCES PHAGOCYTOSIS, IS DETECTED SPECIFICALLY IN HUMAN-CELLS OF MYELOID LINEAGE, ENDOTHELIAL-CELLS, AND PLATELETS

The complement component C1q can interact with a variety of different cells, resulting in multiple functional consequences depending on the cell type. mAbs R3 and R139, which recognize a 126,000 M-r (reduced) c ell surface protein, are able to abrogate the C1q-mediated enhancement of monocyte phagocytosis. The cDNA encoding this C1q receptor that mo dulates phagocytosis, C1qR(p), has recently been cloned. Using a DNA p robe based on the coding region of the receptor, Northern blot and RT- PCR analysis of RNA isolated from different cell types showed C1qR(p) expression in cells of myeloid origin and in endothelial cells, but no t in cells of lymphoid origin nor in the HeLa epithelial-like cell lin e or iliac artery smooth muscle cells. FAGS analysis of cell surface e xpression of C1qR(p), as detected by mAb R139 and R3, corresponded in all cases to the mRNA levels detected. Using the anti-C1qR(p) mAb, the 126,000 M-r receptor was also detected in lysates of human platelets, Interestingly, C1qR(p) is not expressed by the promyelocytic leukemia cell line HL-60, and differentiation of these cells with various chem ical compounds did not induce C1qR(p) expression. It has been reported that C1q can induce specific receptor-mediated responses in fibroblas ts, However, RNA and cell surface expression analysis for C1qR(p) indi cate that this particular C1q receptor is not expressed by either huma n gingival or human skin fibroblasts, These data demonstrate selective expression of C1qR(p) in specific cell types and support the hypothes is that there is more than one C1q receptor mediating the diverse resp onses triggered by C1q.