Association of the 1082 G/A promoter polymorphism of
interleukin - 10 gene with the antibodies production in
patients with rheumatoid arthritis

J 2009

Association of the 1082 G/A promoter polymorphism of interleukin - 10 gene with the antibodies production in patients with rheumatoid arthritis

NĚMEC, Petr; Monika PAVKOVA-GOLDBERGOVA; Jindra GATTEROVA; Zdeněk FOJTÍK; Anna VAŠKŮ et al.

Základní údaje

Originální název

Association of the 1082 G/A promoter polymorphism of interleukin - 10 gene with the antibodies production in patients with rheumatoid arthritis

Název česky

Vztah polymorfismu 1082 G/A promotor genu interleunin-10 a produkce protilátek u pacientů s revmatoidní artritidou

Autoři

NĚMEC, Petr; Monika PAVKOVA-GOLDBERGOVA; Jindra GATTEROVA; Zdeněk FOJTÍK; Anna VAŠKŮ a Miroslav SOUČEK

Vydání

Clin Rheumatol, London, Springer, 2009, 0770-3198

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30102 Immunology

Stát vydavatele

Česká republika

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 1.668

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:14110/09:00039347

Organizační jednotka

Lékařská fakulta

UT WoS

000268102100005

Klíčová slova anglicky

rheumatoid arthritis; Interleukin-10; autoantibodies;

Změněno: 21. 3. 2010 15:01, doc. MUDr. Helena Němcová, CSc.

Anotace

V originále

Interleukin-10 (IL-10) is an immunoregulatory cytokine, usually considered to mediate the downregulation of the inflammatory response in rheumatoid arthritis (RA). Some effects of IL-10 are not anti-inflammatory; for example, the activation of B cells to promote autoantibody production. Allelic polymorphisms located in the promoter region of the IL-10 gene may contribute to the regulation of autoantibodies production. To examine the putative association between the -1082 G/A polymorphism in the promoter region of the IL-10 gene and the susceptibility to disease onset and severity of RA, a total of 144 patients with RA diagnosed according to the revised criteria of the American College of Rheumatology for RA were consecutively recruited into the study. Radiographic progression of RA was scored according to the Sharp/van der Heijde method. Serum levels of rheumatoid factors (RFs) were measured by enzyme-linked immunosorbent assay. Polymerase chain reaction amplification was used for the analysis of the promoter polymorphism of the IL-10 gene. We observed significant differences in genotype distribution of the -1082 G/A polymorphism between IgM RF, IgA RF, and IgG RF positive/negative subgroups of RA patients, with higher prevalence of the GG genotype within IgM RF (Pg = 0.006), IgA RF (Pg = 0.05), and IgG RF (Pg = 0.007) negative RA patients. Results obtained in this study provide the evidence of an association between the -1082 G/A polymorphism in the IL-10 gene promoter and the production of RFs in RA patients.

Citovat

NĚMEC, Petr; Monika PAVKOVA-GOLDBERGOVA; Jindra GATTEROVA; Zdeněk FOJTÍK; Anna VAŠKŮ a Miroslav SOUČEK. Association of the 1082 G/A promoter polymorphism of interleukin - 10 gene with the antibodies production in patients with rheumatoid arthritis. Clin Rheumatol. London: Springer, 2009, roč. 28, č. 8, s. 899-905, 6 s. ISSN 0770-3198.

@article{875450,
   author = {Němec, Petr and PavkovaandGoldbergova, Monika and Gatterova, Jindra and Fojtík, Zdeněk and Vašků, Anna and Souček, Miroslav},
   article_location = {London},
   article_number = {8},
   keywords = {rheumatoid arthritis; Interleukin-10; autoantibodies;},
   language = {eng},
   issn = {0770-3198},
   journal = {Clin Rheumatol},
   title = {Association of the 1082 G/A promoter polymorphism of interleukin - 10 gene with the antibodies production in patients with rheumatoid arthritis},
   volume = {28},
   year = {2009}
}

TY  - JOUR
ID  - 875450
AU  - Němec, Petr - Pavkova-Goldbergova, Monika - Gatterova, Jindra - Fojtík, Zdeněk - Vašků, Anna - Souček, Miroslav
PY  - 2009
TI  - Association of the 1082 G/A promoter polymorphism of interleukin - 10 gene with the antibodies production in patients with rheumatoid arthritis
JF  - Clin Rheumatol
VL  - 28
IS  - 8
SP  - 899-905
EP  - 899-905
PB  - Springer
SN  - 07703198
KW  - rheumatoid arthritis
KW  - Interleukin-10
KW  - autoantibodies;
N2  - Interleukin-10 (IL-10) is an immunoregulatory cytokine, usually considered to mediate the downregulation of the inflammatory response in rheumatoid arthritis (RA). Some effects of IL-10 are not anti-inflammatory; for example, the activation of B cells to promote autoantibody production. Allelic polymorphisms located in the promoter region of the IL-10 gene may contribute to the regulation of autoantibodies production. To examine the putative association between the -1082 G/A polymorphism in the promoter region of the IL-10 gene and the susceptibility to disease onset and severity of RA, a total of 144 patients with RA diagnosed according to the revised criteria of the American College of Rheumatology for RA were consecutively recruited into the study. Radiographic progression of RA was scored according to the Sharp/van der Heijde method. Serum levels of rheumatoid factors (RFs) were measured by enzyme-linked immunosorbent assay. Polymerase chain reaction amplification was used for the analysis of the promoter polymorphism of the IL-10 gene. We observed significant differences in genotype distribution of the -1082 G/A polymorphism between IgM RF, IgA RF, and IgG RF positive/negative subgroups of RA patients, with higher prevalence of the GG genotype within IgM RF (Pg = 0.006), IgA RF (Pg = 0.05), and IgG RF (Pg = 0.007) negative RA patients. Results obtained in this study provide the evidence of an association between the -1082 G/A polymorphism in the IL-10 gene promoter and the production of RFs in RA patients.
ER  -

NĚMEC, Petr; Monika PAVKOVA-GOLDBERGOVA; Jindra GATTEROVA; Zdeněk FOJTÍK; Anna VAŠKŮ a Miroslav SOUČEK. Association of the 1082 G/A promoter polymorphism of interleukin - 10 gene with the antibodies production in patients with rheumatoid arthritis. \textit{Clin Rheumatol}. London: Springer, 2009, roč.~28, č.~8, s.~899-905, 6 s. ISSN~0770-3198.

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