Abstract
Raji cells active the alternative complement pathway (ACP) and fix C3 fragments when incubated in human serum (HS). Earlier experiments have shown that CR2 molecules are involved in this phenomenon and the opsonized cells have elevated sensitivity to the lytic effect of CR3-bearing NK cells. We show here that Raji cells treated with CR2 site-specific ligands, (C3d, OKB-7 and HB-5 mAbs, and a synthetic peptide which binds to CR2) generated and bound C3 fragments after exposure to HS. The elevated lytic sensitivity of HS-treated cells was not altered by the presence of the various CR2 ligands. Thus, the membrane-bound C3 fragments are not fixed at the C3dg receptor binding site.
Original language | English |
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Pages (from-to) | 303-306 |
Number of pages | 4 |
Journal | Immunology Letters |
Volume | 21 |
Issue number | 4 |
DOIs | |
State | Published - 15 Jun 1989 |
Keywords
- C3
- Complement
- CR2