Polymorphisms of the toll-like receptor 9 (TLR9) gene with systemic lupus erythematosus in Chinese

Abstract Toll-like receptor 9 (TLR9) is an important component of the innate immune system and have been associated with several autoimmune diseases, such as Systemic Lupus Erythematosus (SLE). The aim of this study was to investigate polymorphisms in TLR9 gene in a Brazilian SLE patients group and their association with clinical manifestation, particularly Jaccoud’s arthropathy (JA). We analyzed DNA samples from 204 SLE patients, having a subgroup of them presenting JA (n=24). A control group (n=133) from the same city was also included. TLR9 single nucleotide polymorphisms (SNPs) (−1237 C>T and +2848 G>A) were identified by sequencing analysis. The TLR9 gene genotype frequency was similar both in SLE patients and the control group. In the whole SLE population, an association between the homozygosis of allele C at position −1237 with psychosis and anemia (p < 0.01) was found. Likewise, the homozygosis of allele G at position +2848 was associated with a discoid rash (p < 0.05). There was no association between JA and TLR9 polymorphisms. These data show that TLR9 polymorphisms do not seem to be a predisposing factor for SLE in the Brazilian population, and that SNPs are not associated with JA.

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Association study of a single nucleotide polymorphism in the exon 2 region of toll-like receptor 9 (TLR9) gene with susceptibility to systemic lupus erythematosus among Chinese

Molecular Biology Reports ◽

10.1007/s11033-008-9440-z ◽

2009 ◽

Vol 36 (8) ◽

pp. 2245-2248 ◽

Cited By ~ 33

Author(s):

Chang-Juan Xu ◽

Wen-Hui Zhang ◽

Hai-Feng Pan ◽

Xiang-Pei Li ◽

Jian-Hua Xu ◽

...

Keyword(s):

Systemic Lupus Erythematosus ◽

Single Nucleotide Polymorphism ◽

Association Study ◽

Lupus Erythematosus ◽

Toll Like Receptor ◽

Nucleotide Polymorphism ◽

Systemic Lupus ◽

Single Nucleotide ◽

Exon 2 ◽

Tlr9 Gene

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Faculty Opinions recommendation of Dysfunctional interferon-alpha production by peripheral plasmacytoid dendritic cells upon Toll-like receptor-9 stimulation in patients with systemic lupus erythematosus.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1131993.589997 ◽

2008 ◽

Author(s):

Gary Firestein ◽

Susan Sweeney

Keyword(s):

Systemic Lupus Erythematosus ◽

Dendritic Cells ◽

Interferon Alpha ◽

Lupus Erythematosus ◽

Plasmacytoid Dendritic Cells ◽

Toll Like Receptor ◽

Systemic Lupus ◽

Alpha Production

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RNA sensing by conventional dendritic cells is central to the development of lupus nephritis

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1507052112 ◽

2015 ◽

Vol 112 (45) ◽

pp. E6195-E6204 ◽

Cited By ~ 34

Author(s):

Teja Celhar ◽

Richard Hopkins ◽

Susannah I. Thornhill ◽

Raquel De Magalhaes ◽

Sun-Hee Hwang ◽

...

Keyword(s):

Systemic Lupus Erythematosus ◽

Dendritic Cells ◽

Lupus Nephritis ◽

Lupus Erythematosus ◽

Moderate Increase ◽

Rna Recognition ◽

Toll Like Receptor ◽

Systemic Lupus ◽

Slow Progression ◽

Inflammatory Milieu

Glomerulonephritis is a common and debilitating feature of systemic lupus erythematosus (SLE). The precise immune mechanisms that drive the progression from benign autoimmunity to glomerulonephritis are largely unknown. Previous investigations have shown that a moderate increase of the innate Toll-like receptor 7 (TLR7) is sufficient for the development of nephritis. In these systems normalization of B-cell TLR7 expression or temporal depletion of plasmacytoid dendritic cells (pDCs) slow progression; however, the critical cell that is responsible for driving full immunopathology remains unidentified. In this investigation we have shown that conventional DC expression of TLR7 is essential for severe autoimmunity in the Sle1Tg7 model of SLE. We show that a novel expanding CD11b+ conventional DC subpopulation dominates the infiltrating renal inflammatory milieu, localizing to the glomeruli. Moreover, exposure of human myeloid DCs to IFN-α or Flu increases TLR7 expression, suggesting they may have a role in self-RNA recognition pathways in clinical disease. To our knowledge, this study is the first to highlight the importance of conventional DC-TLR7 expression for kidney pathogenesis in a murine model of SLE.

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Serum vitamin D/25(OH)D associated with toll-like receptor (TLR) 2 expression of immune cells in the saliva of Systemic Lupus Erythematosus: a preliminary study

Journal of Oral Medicine and Oral Surgery ◽

10.1051/mbcb/2020062 ◽

2021 ◽

Vol 27 (2) ◽

pp. 22

Author(s):

Hendri Susanto ◽

Bagus Soebadi ◽

Diah Savitri Ernawati ◽

Adiastuti Endah Pamardiati ◽

Hening Tuti Hendarti ◽

...

Keyword(s):

Systemic Lupus Erythematosus ◽

Vitamin D ◽

Immune Cells ◽

Lupus Erythematosus ◽

Serum Vitamin ◽

Toll Like Receptor ◽

Systemic Lupus ◽

Tlr2 Expression ◽

Cross Sectional ◽

Serum Vitamin D

Objective: Vitamin D deficiency may contribute to Systemic Lupus Erythematosus (SLE) development. Vitamin D may involve in pathogen recognition through Toll-like receptor (TLR) 2 in immune cells in saliva. This study aimed to determine the correlation between serum vitamin D/25(OH)D and TLR2 expression of immune cells in the saliva of SLE. Materials and methods: This cross-sectional study conducted at the the SLE patients who met the inclusion and exclusion criteria. Those who had signed informed consent involved to underwent unstimulated saliva collection and blood samples for TLR2 and vitamin D/25(OH)D examination. The correlation between serum vitamin D/25(OH)D concentration and salivary TLR2 expression was analyzed using the correlation test, linear regression with 95% confidence level. Results: Thirty SLE patients had a mean serum vitamin D/25(OH)D concentration of 9.98 ± 4.64 ng/ml. The mean of TLR2 expression of CD11b+ cells in saliva was 26.03 ± 20.92%. There was a significant positive correlation between serum vitamin D/25(OH)D concentration and TLR 2 expression of CD11b+ cells in the saliva. (r = 0.434; P < 0.05). Vitamin D/25(OH)D was the only predictor for TLR 2 expression. Conclusion: Serum vitamin D/25(OH)D concentrations associated with TLR2 expression of CD11b+ cells in the saliva of SLE.

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