PMID- 8299225
OWN - NLM
STAT- MEDLINE
DCOM- 19940309
LR  - 20190821
IS  - 0090-1229 (Print)
IS  - 0090-1229 (Linking)
VI  - 70
IP  - 2
DP  - 1994 Feb
TI  - Relationship between immune complex binding and release and the quantitative 
      expression of the complement receptor, type 1 (CR1, CD35) on human erythrocytes.
PG  - 104-13
AB  - Primate erythrocytes (E) play a central role in clearing potentially pathogenic 
      immune complexes (IC) from the circulation. E capture circulating IC via 
      interaction between C3b and C4b sites, generated on the IC during activation of 
      the complement cascade, and the complement receptor, type 1 (CR1), expressed on 
      E. IC are released from E when C3b and C4b sites on the IC are cleaved by Factor 
      I. The goal of this study was to examine the interactions between human E and 
      model IC in the context of quantitative variations in CR1 expression. IC were 
      prepared by combining murine monoclonal IgG1, IgG2b, or IgG3 anti-dinitrophenyl 
      (DNP) antibodies with DNP-bovine serum albumin. The expression of CR1 on E, 
      obtained from eight healthy donors, was quantified by radioimmunoassay and 
      Scatchard analysis. On the basis of quantitative CR1 expression, preparations of 
      E obtained from different donors at various times were categorized into 
      phenotypic groups expressing high, intermediate, or low numbers of CR1. While 
      there was some variation in the expression of CR1 of individual donors, five of 
      the eight donors remained within the same phenotypic group upon repeated 
      sampling. Surprisingly, when interactions between IC and E were examined in 
      vitro, there was no direct relationship between the number of CR1 per E and the 
      peak magnitude of IC binding to E. When peak binding and release rates were 
      calculated, there was a direct correlation between the number of CR1 per E and 
      the peak binding rate of IC constructed with IgG3 antibodies (IgG3 IC). In 
      addition, there was an inverse correlation between the number of CR1 per E and 
      the peak release rate of IgG2b IC. There was no direct correlation between the 
      quantitative expression of CR1 on E and the peak binding or release rates of IgG1 
      IC. These data indicate that the quantitative expression of CR1 can affect the 
      interactions between IC and E, but that these interactions are also dependent 
      upon the immunochemical properties of the IC. These findings may be relevant to 
      the pathogenesis of diseases, including systemic lupus erythematosus and AIDS, in 
      which E express reduced numbers of CR1.
FAU - Gibson, N C
AU  - Gibson NC
AD  - Department of Microbiology and Immunology, University of Oklahoma Health Sciences 
      Center, Oklahoma City 73190.
FAU - Waxman, F J
AU  - Waxman FJ
LA  - eng
GR  - R01 AI25964/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Clin Immunol Immunopathol
JT  - Clinical immunology and immunopathology
JID - 0356637
RN  - 0 (Antigen-Antibody Complex)
RN  - 0 (Receptors, Complement 3b)
SB  - IM
MH  - Antigen-Antibody Complex/*metabolism
MH  - Erythrocytes/*immunology
MH  - Humans
MH  - In Vitro Techniques
MH  - Receptors, Complement 3b/*metabolism
EDAT- 1994/02/01 00:00
MHDA- 1994/02/01 00:01
CRDT- 1994/02/01 00:00
PHST- 1994/02/01 00:00 [pubmed]
PHST- 1994/02/01 00:01 [medline]
PHST- 1994/02/01 00:00 [entrez]
AID - S0090122984710178 [pii]
AID - 10.1006/clin.1994.1017 [doi]
PST - ppublish
SO  - Clin Immunol Immunopathol. 1994 Feb;70(2):104-13. doi: 10.1006/clin.1994.1017.