Association of TGF-β1 +869C/T promoter polymorphism with susceptibility to autoimmune diseases: a meta-analysis

Abstract

Many case-control studies have investigated the role of TGF-β1 gene +869C/T promoter polymorphism in autoimmune diseases, but the results are inconsistent. To clarify this point, we performed a meta-analysis based on all available studies in Pubmed, Elsevier Science Direct, Google Searching, Chinese Biomedical Literature Database, Chinese National Knowledge Infrastructure. Crude odds ratios (ORs) with 95% confidence intervals were calculated to estimate the strength of the association. A fixed or random effects model was used on the basis of heterogeneity. A total of 21 papers including 2,693 cases and 3,036 controls were considered in the current meta-analysis. These studies encompass two ankylosing spondylitis (AS), eight rheumatoid arthritis (RA), four systemic lupus erythematosus (SLE), and seven systemic sclerosis (SSc). The results showed that TGF-β1 +869C/T promoter polymorphism were associated with susceptibility to RA (CC vs. TT: OR=0.65, 95% CI=0.48-0.88, P=0.005; CC vs. CT+TT: OR=0.56, 95% CI=0.45-0.69, P=0.000; C vs. T: OR=0.81, 95% CI=0.71-0.93, P=0.003). When stratified by race, significant association was observed only in Asian population. However, we failed to reveal the association between this gene promoter polymorphism and AS, SLE, and SSc. Therefore, this meta-analysis suggests a possible association between TGF-β1 +869C/T promoter polymorphism and RA, especially in Asian population.

Genetic Case-Control Study for Eight Polymorphisms Associated with Rheumatoid Arthritis

“…They concluded that T869C was associated with RA in Asian patients but not in non-Asian patients [ 39 ]. This conclusion was confirmed by Zhang et al [ 40 ]. The (TT) genotype represented a risk factor for RA while (CC) genotype or (C) allele seemed to be protective to RA through a meta-analysis conducted by Zhou et al [ 41 ].…”

Interleukin 10 and transforming growth factor beta 1 gene polymorphisms in juvenile idiopathic arthritis

“…On the contrary, Cinek et al did not recognize any association between TGF-β1 SNPs and JIA proneness in Czech population (28). Two meta-analysis studies carried out by Chang et al (29) and Zhang et al (30) divulged an association between TGF-β1 T869C polymorphism and RA in the people of Asian descent, but not in the people of non-Asian descent. On the other hand, our fi ndings are not in line with the investigation performed by Hussein et al, who found the TGF-β1 T allele at codon 10 to be associated with susceptibility to RA (25).…”

Kandidātgēnu polimorfismu saistība ar ankilozējošo spondilītu un tā klīnisko gaitu. Promocijas darbs

“…Lokāli tam ir pretiekaisuma darbība, savukārt sistēmiski ir imūnsupresīvs efekts (Howe et al, 2005).TGFβ1 gēns atrodas19. hromosomā (19q13.2), sastāv no septiņiem eksoniem un sešiem introniem un kodē TGFβ proteīnu saimes ligandu(Zhang et al, 2013). Šīs saimes ligandi, saistoties ar TGFβ receptoriem, izraisa transkripcijas faktoru piesaisti un aktivāciju, kas regulē gēnu ekspresiju(Blobe et al, 2000).…”

“…Pētījumos tiek analizēta tā saistībā ar dažāda veida ļaundabīgiem audzējiem, koronāro sirds slimību, periodontītu, kaulu minerālo blīvumu, hronisko obstruktīvo plaušu slimību, IgA nefropātiju utt. Pēdējo gadu desmitos ir veikti pētījumi, lai noteiktu TGFβ1 polimorfismu saistību ar RA, SSV, sistēmas sklerozi, 1. tipa cukura diabētu un AS, bet dati ir pretrunīgi(Zhang et al, 2013).2013. gadā veiktajā metaanalīzē par TGFβ1 +869C/T (rs1800470) saistību ar vairākām ar imūno sistēmu saistītām slimībām, ieskaitot AS (pacienti no Nīderlandes un Ķīnas dienvidiem), netika iegūti asociāciju ar AS apstiprinošie dati(Zhang et al, 2013).…”

“…Pēdējo gadu desmitos ir veikti pētījumi, lai noteiktu TGFβ1 polimorfismu saistību ar RA, SSV, sistēmas sklerozi, 1. tipa cukura diabētu un AS, bet dati ir pretrunīgi(Zhang et al, 2013).2013. gadā veiktajā metaanalīzē par TGFβ1 +869C/T (rs1800470) saistību ar vairākām ar imūno sistēmu saistītām slimībām, ieskaitot AS (pacienti no Nīderlandes un Ķīnas dienvidiem), netika iegūti asociāciju ar AS apstiprinošie dati(Zhang et al, 2013). Savukārt 2005. gadā veiktā pētījuma dati ar angļu (no Lielbritānijas) un somu ģimenēm (no Somijas) norādīja par TGFβ1 polimorfismu mazu nozīmi AS patoģenēzē (no 5 pētītiem SNPs tikai +1632C/T bija vāja asociācija ar AS) (Jaakkola et al, 2004).…”