| The role of complement receptor type 1 (CR1, CD35) in determining the cellular distribution of opsonized immune complexes between whole blood cells: kinetic analysis of the buffering capacity of erythrocytes. | |
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MedLine Citation:
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PMID: 9038723 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Erythrocytes (E) express complement receptor, type 1 (CR1, CD35), by which they bind opsonized immune complexes (IC) in competition with leucocytes expressing higher numbers of CR1 as well as other complement- and Fc-receptors. This may prevent inappropriate activation of phagocytic cells. We examined the distribution on whole blood cells of preformed tetanus toxoid (TT)/human anti-TT IC, opsonized in situ in 80% autologous serum. Binding to E occurred rapidly and reflected the kinetics of C3-fragment incorporation into the IC. Among eight donors, expressing 180-361 CR1 per E. > 90% of the cell-bound IC were associated with E from 1 to 5 min of incubation, decreasing to 12 +/- 13% after 40 min. Upon comparison of the IC-binding to leucocytes in whole blood with that of isolated leucocytes we found that E, despite their extensive early complex uptake, only reduced the IC-deposition on polymorphonuclear leucocytes (PMN) by 61 +/- 26% after 30 seconds of incubation and 47 +/- 14% after 5 min. During the subsequent 10 min, this buffering capacity of E was essentially abolished E restricted the initial IC-binding to B cells by 73 +/- 19%, but from 3 min of incubation the presence of E promoted, in a CR1-dependent manner, a progressive uptake via CR2 by the B cells. CR1 was the dominant receptor in the early IC-uptake by B cells as well as PMN and monocytes, since CR1-blockade inhibited the initial IC-uptake by these populations in a preparation of isolated leucocytes suspended in serum by > or = 84% after 30 seconds of incubation. We conclude, that E exert a substantial buffering effect on the IC-deposition on PMN, monocytes and B cells, while CR1 is the dominant receptor in the uptake by these cells. However, this effect is short-lived and less than expected from the proportion of IC bound to E. Moreover, E are efficient processors of IC-attached C3b/iC3b fragments to C3dg as indicated by a pronounced enhancement by E of IC-uptake via CR2 on B cells. We propose that this mechanism may play a role in preventing phagocyte activation via CR3. |
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Authors:
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C H Nielsen; S H Matthiesen; I Lyng; R G Leslie |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Immunology Volume: 90 ISSN: 0019-2805 ISO Abbreviation: Immunology Publication Date: 1997 Jan |
Date Detail:
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Created Date: 1997-03-07 Completed Date: 1997-03-07 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 0374672 Medline TA: Immunology Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 129-37 Citation Subset: IM |
Affiliation:
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Department of Medical Microbiology, Odense University, Denmark. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Antigen-Antibody Complex / immunology*, metabolism B-Lymphocytes / immunology Cell Culture Techniques Erythrocytes / immunology* Female Humans Male Monocytes / immunology Neutrophils / immunology Phagocytosis / immunology* Receptors, Complement 3b / immunology* Tetanus Toxoid / immunology |
| Chemical | |
Reg. No./Substance:
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0/Antigen-Antibody Complex; 0/Receptors, Complement 3b; 0/Tetanus Toxoid |
| Comments/Corrections | |
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