HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Carlo, J. R. Articles by Conrad, D. H. Search for Related Content PubMed Articles by Carlo, J. R. Articles by Conrad, D. H.

Complement Receptor Binding of C3b-Coated Cells Treated with C3b Inactivator, 1H Globulin and Trypsin¹

From the Department of Medicine, Division of Immunology and Connective Tissue Diseases and the Department of Microbiology, Medical College of Viriginia, Richmond, Virginia 23298

Abstract

Treatment of ¹²⁵I-C3b bound to EAC1423b with C3b inactivator (C3bINA) and 1H globulin (1H) cleaved the -chain of C3b into 65,000- and 42,000-dalton fragments, both of which remained disulfide-bonded to the intact -chain (C3bi). Subsequent treatment with trypsin (0.1 µg/ml) released ¹²⁵I into the supernatant and yielded cells coated with a 33,000-dalton fragment of -chain, presumably C3d. These results are in agreement with those obtained by others using fluid phase C3b. C3b-coated cells (EAC1423b) adhered to complement (C) receptors on human erythrocytes, glomeruli, and monocytes. C3bi-coated cells adhered to the receptors on glomeruli and monocytes, but not to those on human erythrocytes. C3d-coated cells adhered only to the monocyte receptors. The findings suggest that the glomerular C receptor recognizes portions of the C3 molecule different from those recognized by either the erythrocyte or monocyte receptors.

Footnotes

¹ This work was supported by NIH Grants AI 13049, AM 18976, and T32 AM 07079; an Arthritis Clinical Research Center Grant from the Arthritis Foundation, Atlanta, Georgia; and an A. D. Williams Grant from the Medical College of Virginia. This is publication No. 130 from the Charles W. Thomas Arthritis Fund, Medical College of Viriginia.