Deficiency of complement-dependent prevention of immune precipitation in systemic sclerosis
Autor: | Arni Jon Geirsson, R Kolka, T. Vikingsdottir, Helgi Valdimarsson, G J Arason |
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Rok vydání: | 2002 |
Předmět: |
Adult
Male Adolescent Concise Report Immunology Enzyme-Linked Immunosorbent Assay chemical and pharmacologic phenomena macromolecular substances General Biochemistry Genetics and Molecular Biology Immunoenzyme Techniques Classical complement pathway Immune system Rheumatology Antibody Specificity Immunopathology Humans Immunology and Allergy Medicine Complement Pathway Classical skin and connective tissue diseases Immunoelectrophoresis Complement C1q Aged Aged 80 and over Electrophoresis Agar Gel Scleroderma Systemic integumentary system business.industry musculoskeletal neural and ocular physiology C4A Complement C4 Complement C3 Middle Aged Immune complex Complement system Precipitins nervous system Case-Control Studies Humoral immunity Female business |
Zdroj: | Annals of the Rheumatic Diseases. 61:257-260 |
ISSN: | 0003-4967 |
DOI: | 10.1136/ard.61.3.257 |
Popis: | Previous studies have indicated that complement may be activated or inherently abnormal in systemic sclerosis (SSc), and it has been suggested that immune complex deposition plays a part in the microvascular damage of this disease.To study several aspects of the complement system in 24 patients with SSc.Complement dependent prevention of immune precipitation (PIP) was measured by a sensitive enzyme immunoassay, levels of C1q, C4, and C3 by rocket immunoelectrophoresis, C4 allotypes by high voltage agarose electrophoresis, and C4A, C4B, and C3d by an enzyme linked immunosorbent assay (ELISA).PIP was markedly decreased in the patients with SSc (p0.001). Abnormal complement activation was detected in nine patients as raised levels of the complement split product C3d. However, a relation between low PIP and complement activation was not seen. PIP was significantly lower in patients who carried the C4A*Q0 allotype (p=0.03), and a strong correlation was found between PIP and C4A concentration (p0.00001). The PIP defect may, at least in some patients, be associated with the initial phase of the disease.The results show a previously unrecognised functional defect of complement in SSc; the defect correlates with low levels of classical pathway components and, in particular, C4A. |
Databáze: | OpenAIRE |
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