Abstract
Toll-like receptors (TLRs) are a family of transmembrane receptors, and play a vital role in recognizing invading pathogens and activating innate immunity. Previous studies indicated that TLR1 single nucleotide polymorphisms (SNPs) might be associated with the risk of IgA nephropathy (IgAN). This study aims to investigate the relationship between TLR1 SNPs (rs4833095 and rs5743557) and IgAN in a Chinese Han population. This case-control study included 351 patients with IgAN and 310 healthy controls. Two SNPs (rs4833095 and rs5743557) of TLR1 were genotyped by Sequenom MassARRAY. Odds ratios (OR) with 95% confidence intervals (CI) were used to assess the relationship with IgAN. We found that both allele and genotype frequencies of rs5743557 were not associated with IgAN risk. Rs4833095 increased IgAN risk compared with controls in the allele, dominant and log-additive models (P = 0.04, 0.04 and 0.03, respectively). Further haplotype analysis revealed that the Trs4833095Trs5743557 haplotype may be a risk factor for IgAN (OR = 1.28; 95% CI = 1.01–1.63; P = 0.046). Furthermore, rs4833095 was associated with Lee's grades (OR = 1.75; 95% CI = 1.03–2.96; P = 0.04). However, there was no significant association between the genotype distributions of rs5743557 and clinical parameters of IgAN such as gender, 24 hour urine protein, blood pressure, and Lee's grades. Taken together, these findings suggest that the TLR1 rs4833095 polymorphism may play a role in the development and progression of IgAN.
Highlights
IgA nephropathy (IgAN) is a common form of primary glomerulonephritis worldwide [1] and was first described in 1968 by Berger [2]
Toll-like receptors (TLRs) are a family of receptors that belong to type I membrane glycoproteins
TLR1 is expressed in glomerular mesangial cells [24] and tubular epithelial cells to activate the immune responses during tubulointerstitial injuries [25]
Summary
IgA nephropathy (IgAN) is a common form of primary glomerulonephritis worldwide [1] and was first described in 1968 by Berger [2]. It is widely acknowledged that, in patients with IgAN, the mesangium IgA deposits are exclusively of the IgA1 subclass and often present with abnormal glycosylation [3, 4]. This phenomenon has been found to be the consequence of abnormal systemic responses to mucosally encountered antigens in IgAN patients [5]. Mucosal immunity is often triggered by receptors that can recognize pathogen associated molecular patterns expressed in pathogens of bacterial, viral, and fungal origins [6]. Toll-like receptors (TLRs) are the most frequent pattern recognition receptors [7,8,9]
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