Type I IgE receptor, interleukin 4 receptor and interleukin 13 polymorphisms in children with nephrotic syndrome

2002 ◽  
Vol 102 (5) ◽  
pp. 507 ◽  
Author(s):  
K. TENBROCK ◽  
A. SCHUBERT ◽  
L. STAPENHORST ◽  
M. J. KEMPER ◽  
J. GELLERMANN ◽  
...  
2002 ◽  
Vol 102 (5) ◽  
pp. 507-512 ◽  
Author(s):  
K. TENBROCK ◽  
A. SCHUBERT ◽  
L. STAPENHORST ◽  
M.J. KEMPER ◽  
J. GELLERMANN ◽  
...  

Polymorphisms in the genes encoding the high-affinity IgE receptor, the interleukin 4 (IL4) receptor and IL13 can be associated with the development of asthma and allergy. Although several studies have described an association between atopy and idiopathic childhood nephrotic syndrome (NS), it is not clear whether this association is of a causal nature. Furthermore, it is not known whether these polymorphisms are associated with the clinical course of NS. A total of 84 children (52 male and 32 female; mean age 12.1 years) with NS were included in the present study. Of these, 78 could be classified as either atopic or non-atopic. Atopy was defined by elevated IgE levels (>100k-units/l) and/or a positive history of atopy (33 of 78 patients). DNA was extracted from blood collected in EDTA tubes, and polymorphisms at positions 50 and 551 of the IL4 receptor, position 110 of IL13 and position 181 of the high-affinity IgE receptor were investigated by sequence-specific PCR or direct sequencing. Although we noted a strong tendency towards a higher allele frequency of polymorphisms in children with atopy and NS compared with children with NS but without atopy (IL4 50, 30% compared with 18%; IL4 551, 39% compared with 31%; IL13 110, 45% compared with 33%; IgE 181, 12% compared with 13%), these differences did not reach statistical significance. There were no differences in the frequency of polymorphisms between the different clinical courses of NS (frequent relapsers, steroid-dependent or steroid-resistant NS). We conclude that polymorphisms in the IL4 receptor, the high-affinity IgE receptor and IL13 do not seem to predict the clinical course of NS, despite the fact that serum IgE elevations are more frequent in patients with NS than in normal control subjects. The investigated polymorphisms may contribute to the IgE switch in patients with NS.


2010 ◽  
Vol 153 (3) ◽  
pp. 259-267 ◽  
Author(s):  
Renske W.B. Bottema ◽  
Ilja M. Nolte ◽  
Timothy D. Howard ◽  
Gerard H. Koppelman ◽  
Anthony E.J. Dubois ◽  
...  

1995 ◽  
Vol 270 (8) ◽  
pp. 3512-3517 ◽  
Author(s):  
Natalio Vita ◽  
Sylvie Lefort ◽  
Patrick Laurent ◽  
Daniel Caput ◽  
Pascual Ferrara

1996 ◽  
Vol 93 (1) ◽  
pp. 497-501 ◽  
Author(s):  
D. J. Hilton ◽  
J. G. Zhang ◽  
D. Metcalf ◽  
W. S. Alexander ◽  
N. A. Nicola ◽  
...  

2020 ◽  
Vol 82 (9) ◽  
pp. 1253-1259
Author(s):  
Kazuaki TANAKA ◽  
Misaki YAMAMOTO-FUKUDA ◽  
Tatsuya TAKIZAWA ◽  
Hidekatsu SHIMAKURA ◽  
Masahiro SAKAGUCHI

2013 ◽  
Vol 9 (12) ◽  
pp. 3009 ◽  
Author(s):  
Allison-Lynn Andrews ◽  
Ida Karin Nordgren ◽  
Gemma Campbell-Harding ◽  
John W. Holloway ◽  
Stephen T. Holgate ◽  
...  

2016 ◽  
Vol 61 (1) ◽  
pp. 40-45 ◽  
Author(s):  
Beata Narożna ◽  
Aleksandra Hoffmann ◽  
Paulina Sobkowiak ◽  
Natalia Schoneich ◽  
Anna Bręborowicz ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
T. M. Brombacher ◽  
I. Berkiks ◽  
S. Pillay ◽  
M. Scibiorek ◽  
B. O. Moses ◽  
...  

Abstract Like pro-inflammatory cytokines, the role of anti-inflammatory cytokines in both learning and memory has been investigated, revealing beneficial effects for both interleukin-4 and interleukin-13 via the common interleukin-4 receptor alpha chain complex. In this study, using the Morris water maze spatial task for cognition, we compared interleukin-4 receptor alpha- deficient mice and their ligands interleukin-4/ interleukin-13 double deficient mice, on a Balb/c background. We demonstrate that while interleukin-4/ interleukin-13 double deficient mice are significantly impaired in both learning and reference memory, interleukin-4 receptor alpha-deficiency impairs only reference memory, compared to the wild-type control mice. In order to better understand how interleukin-4 receptor alpha- deficient mice are able to learn but not remember, we investigated the BDNF/TrkB- and the ARC-signaling pathways. We show that interleukin-4 receptor alpha-deficiency disrupts activation of BDNF/TrkB- and ARC-signaling pathways during reference memory, while the pathway for spatial learning is spared.


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