Abstract:
:A complete functional deficiency of C1q is described in a patient suffering from SLE. From reduced plasma C1 activity of the parents a hereditary trait was assumed. The defective C1q molecule was haemolytically inactive, did not bind to immune complexes, and was not recognized by the monocyte C1q receptor. C1 activity in the patient's serum could be restored by the addition of purified C1q. Analysis by gel-filtration and ultracentrifugation experiments revealed an immunoreactive molecule of about 150 kD mol. wt, corresponding to one structural subunit of the C1q macromolecule, containing two A chain-B chain dimers and a C-C chain dimer. Applying Southern blot analysis with cDNA clones encoding for the three individual chains of the C1q molecule, no restriction fragment length polymorphism was detected, ruling out possible major alterations of the genetic information.
journal_name
Clin Exp Immunoljournal_title
Clinical and experimental immunologyauthors
Kirschfink M,Petry F,Khirwadkar K,Wigand R,Kaltwasser JP,Loos Mdoi
10.1111/j.1365-2249.1993.tb03442.xsubject
Has Abstractpub_date
1993-11-01 00:00:00pages
267-72issue
2eissn
0009-9104issn
1365-2249journal_volume
94pub_type
杂志文章abstract::During routine immunofluorescence studies of the serum of a patient with Sjögren's syndrome and lymphoma we detected antibodies giving a cytoplasmic pattern which did not correspond to previously described patterns found for autoantibodies. Using different cells and tissues as substrates for indirect immunofluorescenc...
journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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doi:
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journal_title:Clinical and experimental immunology
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journal_title:Clinical and experimental immunology
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