Binding of immune complexes to erythrocyte CR1 (CD35): difference in requirement of classical pathway components and indication of alternative pathway-mediated binding in C2-deficiency
(2000) In Scandinavian Journal of Immunology 52(1). p.103-108- Abstract
- Deficiency of complement components within the classical pathway is associated with increased risk for immune complex disease. However, C2-deficient individuals often have a mild disease and about 50% are healthy. To study the importance of the different components for immune complex clearance, bovine serum albumin (BSA)/anti-BSA complexes were opsonized in human serum and the binding to erythrocyte complement receptor type 1 (CR1, CD35) was measured in vitro. In C2-depleted serum the complexes were opsonized and bound to CR1 but the reaction needed a longer opsonization time than in normal human serum (NHS). In contrast, serum reagent lacking C1q, C4 or C3 did not promote binding in this assay system. We also demonstrated that elevated... (More)
- Deficiency of complement components within the classical pathway is associated with increased risk for immune complex disease. However, C2-deficient individuals often have a mild disease and about 50% are healthy. To study the importance of the different components for immune complex clearance, bovine serum albumin (BSA)/anti-BSA complexes were opsonized in human serum and the binding to erythrocyte complement receptor type 1 (CR1, CD35) was measured in vitro. In C2-depleted serum the complexes were opsonized and bound to CR1 but the reaction needed a longer opsonization time than in normal human serum (NHS). In contrast, serum reagent lacking C1q, C4 or C3 did not promote binding in this assay system. We also demonstrated that elevated levels of factor B could restore binding of complexes to erythrocytes in C2-depleted serum via alternative pathway activation. These results indicate that in spite of lack of a complete classical pathway, C2-deficient individuals could retain some immune complex opsonizing activity via the alternative pathway. This finding could contribute to the understanding of differences in association between complement deficiency and immune-complex disease. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1117613
- author
- Klint, Cecilia LU ; Gullstrand, Birgitta LU ; Sturfelt, Gunnar LU and Truedsson, Lennart LU
- organization
- publishing date
- 2000
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scandinavian Journal of Immunology
- volume
- 52
- issue
- 1
- pages
- 103 - 108
- publisher
- Wiley-Blackwell
- external identifiers
-
- pmid:10886790
- scopus:0033931422
- ISSN
- 1365-3083
- DOI
- 10.1046/j.1365-3083.2000.00752.x
- language
- English
- LU publication?
- yes
- id
- fcb3a2a2-4ca1-4783-ab5d-77e201803f82 (old id 1117613)
- date added to LUP
- 2016-04-01 16:28:06
- date last changed
- 2022-01-28 19:55:56
@article{fcb3a2a2-4ca1-4783-ab5d-77e201803f82,
abstract = {{Deficiency of complement components within the classical pathway is associated with increased risk for immune complex disease. However, C2-deficient individuals often have a mild disease and about 50% are healthy. To study the importance of the different components for immune complex clearance, bovine serum albumin (BSA)/anti-BSA complexes were opsonized in human serum and the binding to erythrocyte complement receptor type 1 (CR1, CD35) was measured in vitro. In C2-depleted serum the complexes were opsonized and bound to CR1 but the reaction needed a longer opsonization time than in normal human serum (NHS). In contrast, serum reagent lacking C1q, C4 or C3 did not promote binding in this assay system. We also demonstrated that elevated levels of factor B could restore binding of complexes to erythrocytes in C2-depleted serum via alternative pathway activation. These results indicate that in spite of lack of a complete classical pathway, C2-deficient individuals could retain some immune complex opsonizing activity via the alternative pathway. This finding could contribute to the understanding of differences in association between complement deficiency and immune-complex disease.}},
author = {{Klint, Cecilia and Gullstrand, Birgitta and Sturfelt, Gunnar and Truedsson, Lennart}},
issn = {{1365-3083}},
language = {{eng}},
number = {{1}},
pages = {{103--108}},
publisher = {{Wiley-Blackwell}},
series = {{Scandinavian Journal of Immunology}},
title = {{Binding of immune complexes to erythrocyte CR1 (CD35): difference in requirement of classical pathway components and indication of alternative pathway-mediated binding in C2-deficiency}},
url = {{http://dx.doi.org/10.1046/j.1365-3083.2000.00752.x}},
doi = {{10.1046/j.1365-3083.2000.00752.x}},
volume = {{52}},
year = {{2000}},
}