Authors: Ding, J.-X.; Xu, L.-X.; Zhu, L.; Lv, J.-C.; Zhao, M.-H.; Zhang, H.; Wang, H.-Y.

Source: Scandinavian Journal of Immunology, Volume 69, Number 2, February 2009 , pp. 174-180(7)

Publisher: Wiley-Blackwell

Abstract:

It is known that aberrant sialylation of IgA1 is involved in the pathogenesis of IgA nephropathy (IgAN). We hypothesize that aberrant sialylation of serum IgA1 may result from changes in the activity of α2,6-sialyltransferase (α2,6-ST) or expression of its coding gene ST6GALNAC2 in peripheral B lymphocytes. Sixty patients with IgAN and 20 healthy controls were enrolled. Peripheral B lymphocytes were isolated by CD-19-positive magnetic beads. The expression level of ST6GALNAC2 was quantitatively analysed by real-time reverse-transcriptase polymerase chain reaction (PCR). Serum IgA1 and sialylation levels were detected by enzyme-linked immunosorbent assay (ELISA) and specific lectin-binding ELISA. Activity of α2,6-ST was measured by specific lectin-binding ELISA. Expression of ST6GALNAC2 in B peripheral lymphocytes was significantly lower in patients with IgAN than that in normal controls (3.7 ± 2.2 versus 6.3 ± 2.3, P = 0.016); α2,6-ST activity in B lymphocytes was correlated positively with the level of α2,6-sialic acid in serum IgA1 in patients (n = 42) and controls (n = 12) (r = 0.37, P = 0.007). However, α2,6-ST activity did not differ between patients with IgAN and controls (1.19 ± 1.43 versus 1.06 ± 1.17, P > 0.05). These data suggested that reduced sialylation of serum IgA1 may result from decreased expression of ST6GALNAC2. The factors affecting activity of α2,6-ST in the sialylation of IgA1 need to be further investigated.

Document Type: Research article

DOI: http://dx.doi.org/10.1111/j.1365-3083.2008.02204.x

Publication date: 2009-02-01

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• In this Subject: Microbiology ,  Allergy & Immunology
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