| Autor: |
Gupta, R. C., McDuffie, F. C., Tappeiner, G., Jordon, R. E. |
| Předmět: |
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| Zdroj: |
Immunology; Apr78, Vol. 34 Issue 4, p751-761, 11p |
| Abstrakt: |
We have found that, although the binding of particulate antigen-antibody complement complexes such as EAC to lymphoblastoid Raji cells is mediated largely through receptors for C3b, the binding of complement-containing soluble complexes such as those prepared with aggregated human IgG (AHO) occurs also via receptors for Clq. Evidence supporting this conclusion included: (1) Binding of AHO to Raji cells takes place after incubation in EDTA serum; (2) Binding of AHG does not occur in Clq deficient EDTA serum but does take place after addition of Clq; (3) The extent of binding of AHU in EDTA serum is a function of the amount of Clq present; (4) Raji cells can bind up to 5.4 × 105 molecules of 125I Clq per cell which can be blocked by unlabelled Clq; (5) AHG preincubated with C can bind to a T-cell line MOLT, which lacks receptors for C3b but possesses receptors for Clq to the same extent as Raji cells; (6) Immunoassays for immune complexes in human sera yield similar results whether Raji cells, MOLT cells or Clq precipitation is used for assay; (7) EAC-Raji cell rosettes can be inhibited with inulin-treated, Clq deficient serum containing C3b or C3d whereas binding of AHG or immune complexes in patient samples to Raji or MOLT cells is not inhibited by this reagent. We conclude that receptors for Clq on certain B and T lymphocytes may play an important role in physiologic functions of lymphocytes depending on binding of soluble immune complexes to their surfaces. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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