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C1q Knock-Out Mice for the Study of Complement Deficiency in Autoimmune Disease

C1q Knock-Out Mice for the Study of Complement Deficiency in Autoimmune Disease In humans, homozygous deficiency of the first component of the classical pathway of complement, C1q, is a powerful disease susceptibility factor for the development of systemic lupus erythematosus (SLE). This strong association indicates that a functional activity of C1q protects from the development of SLE. Studies in vitro have shown that C1q can bind apoptotic keratinocytes suggesting that it may have an important role in the clearance of apoptotic cells. C1q-deficient mice, generated by gene targeting, showed an increased mortality and 25% of the mice had histological evidence of glomerulonephritis characterised by multiple apoptotic cell bodies and immune deposits, assessed by immunofluorescence and electron microscopy. These observations are compatible with the hypothesis that C1q deficiency causes autoimmunity by an impaired clearance of apoptotic cells. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Experimental and Clinical Immunogenetics Karger

C1q Knock-Out Mice for the Study of Complement Deficiency in Autoimmune Disease

Botto, Marina
Experimental and Clinical Immunogenetics , Volume 15 (4): 4 – Feb 1, 1999
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References (15)

Publisher
Karger
Copyright
© 1998 S. Karger AG, Basel
ISSN
0254-9670
eISSN
1421-9948
DOI
10.1159/000019076
Publisher site
See Article on Publisher Site

Abstract

In humans, homozygous deficiency of the first component of the classical pathway of complement, C1q, is a powerful disease susceptibility factor for the development of systemic lupus erythematosus (SLE). This strong association indicates that a functional activity of C1q protects from the development of SLE. Studies in vitro have shown that C1q can bind apoptotic keratinocytes suggesting that it may have an important role in the clearance of apoptotic cells. C1q-deficient mice, generated by gene targeting, showed an increased mortality and 25% of the mice had histological evidence of glomerulonephritis characterised by multiple apoptotic cell bodies and immune deposits, assessed by immunofluorescence and electron microscopy. These observations are compatible with the hypothesis that C1q deficiency causes autoimmunity by an impaired clearance of apoptotic cells.

Journal

Experimental and Clinical Immunogenetics – Karger

Published: Feb 1, 1999

Keywords: Complement; Deficiency; Autoimmunity; Gene targeting; Mice

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