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Hereditary dysfunction of the third component of complement associated with a systemic lupus erythematosus-like syndrome and meningococcal meningitis.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Oncology, Radiology and Clinical Immunology.
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1992 (English)In: Arthritis and Rheumatism, ISSN 0004-3591, E-ISSN 1529-0131, Vol. 35, no 5, 580-586 p.Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE: We describe a dysfunction of C3 in a patient with a systemic lupus erythematosus (SLE)-like syndrome. Alternative pathway complement function was absent, but classical pathway complement function was partially intact.

METHODS: We used functional, preparative, and immunochemical techniques in the study.

RESULTS: The patient's C3 proved normally susceptible to trypsin proteolysis and partially resistant to classical pathway, but completely resistant to alternative pathway, convertase-dependent cleavage.

CONCLUSION: The dysfunction, thus, was caused by a failure of C3 to interact with the C3 convertases, rather than by a lack of a proteinase-sensitive cleavage site in the deficient protein.

Place, publisher, year, edition, pages
1992. Vol. 35, no 5, 580-586 p.
National Category
Medical and Health Sciences
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URN: urn:nbn:se:uu:diva-265465PubMedID: 1575793OAI: oai:DiVA.org:uu-265465DiVA: diva2:865770
Available from: 2015-10-29 Created: 2015-10-29 Last updated: 2017-12-01

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