| Autor: |
Novak J; Department of Microbiology, University of Alabama at Birmingham, 35294, USA. Jan_Novak@microbio.uab.edu, Julian BA, Tomana M, Mesteck J |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of clinical immunology [J Clin Immunol] 2001 Sep; Vol. 21 (5), pp. 310-27. |
| DOI: |
10.1023/a:1012284402054 |
| Abstrakt: |
Several new findings emerged recently from biochemical, genetic, and molecular studies of patients with IgA nephropathy. It appears that immunoglobulin A1-secreting cells of IgA nephropathy patients produce increased amounts of aberrantly glycosylated IgA1 in which the O-linked glycans in the hinge region are deficient in the content of galactose. The galactose-deficient IgA1 in the circulation is recognized by naturally occurring antibodies with anti-glycan specificity, and immune complexes are formed. These circulating immune complexes escape hepatic degradation and eventually are deposited in the kidney mesangium. Resident mesangial cells bind the IgA-containing immune complexes with the involvement of a novel IgA receptor and become activated. A familial form of IgA nephropathy has been linked to chromosome 6q22-23. Recent progress in molecular analyses of IgA nephropathy thus defines this disease as an autoimmune process with a novel IgA mesangial receptor and certain genetically determined traits. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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