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Polymorphism rs3828903 within MICB Is Associated with Susceptibility to Systemic Lupus Erythematosus in a Northern Han Chinese Population.

Zhang YM, Zhou XJ, Cheng FJ, Qi YY, Hou P, Zhao MH, Zhang H - J Immunol Res (2016)

Bottom Line: In silico analyses predicted a higher affinity to transcription factors for allele G (risk) and cis-expression quantitative trait loci (cis-eQTL) effects of rs3828903 in multiple tissues (P ranging from 2.79 × 10(-6) to 6.27 × 10(-38)).Furthermore, higher mRNA expressions of MICB were observed in B cells, monocytes, and renal biopsies from SLE patients compared to controls.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Renal Division, Peking University First Hospital, Beijing 100034, China; Peking University Institute of Nephrology, Beijing 100034, China; Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment, Peking University, Ministry of Education, Beijing 100034, China.

ABSTRACT
Objectives. The variant rs3828903 within MICB, a nonclassical MHC class I chain-related gene, was detected to contribute to systemic lupus erythematosus (SLE) in a Caucasian population. This study aimed to investigate the association in a northern Han Chinese population. Methods. We recruited 1077 SLE patients and 793 controls for analysis. rs3828903 was genotyped by TaqMan allele discrimination assay. Using the public databases, its functional annotations and gene differential expression analysis of MICB were evaluated. Results. Significant association between the allele G of rs3828903 and risk susceptibility to SLE was observed after adjusting for sex and age (P = 1.87 × 10(-2)). In silico analyses predicted a higher affinity to transcription factors for allele G (risk) and cis-expression quantitative trait loci (cis-eQTL) effects of rs3828903 in multiple tissues (P ranging from 2.79 × 10(-6) to 6.27 × 10(-38)). Furthermore, higher mRNA expressions of MICB were observed in B cells, monocytes, and renal biopsies from SLE patients compared to controls. Conclusion. An association between rs3828903 and susceptibility to SLE has been detected in a Chinese population. This together with the functional annotations of rs3828903 converts MICB into a main candidate in the pathogenesis of SLE.

No MeSH data available.


Related in: MedlinePlus

Gene differential expression analyses of MICB in immune cell subsets and renal biopsies from SLE patients and controls. (a)–(h) present the MICB expression levels in immune cell subsets and renal biopsy samples from SLE patients and normal donor controls. MICB mRNA expression was significantly or marginally significantly upregulated in SLE B cells (489.80 ± 95.50 versus 352.66 ± 96.13; P = 1.31 × 10−2; (b)), monocytes (1661.14 ± 532.87 versus 1065.38 ± 220.72; P = 4.97 × 10−2; (e)), tubulointerstitial samples (4.33 ± 0.22 versus 4.21 ± 0.16; P = 7.45 × 10−2; (g)), and glomeruli samples (7.92 ± 0.52 versus 6.77 ± 0.23; P = 2.18 × 10−13; (h)). Although with a rather small sample size, a marginally significantly higher expression level of MICB has been observed in monocytes from healthy donors incubated with SLE sera compared to those incubated with autologous serum (1047.50 ± 494.43 versus 300.40 ± 48.88; P = 5.98 × 10−2; (f)), while there was no difference of MICB mRNA expression in PBMC (1577.45 ± 488.74 versus 1610.67 ± 325.23; P = 0.78; (a)), CD3+ T cells (2195.09 ± 865.77 versus 1900.54 ± 715.70; P = 0.35; (c)), and CD4+ T cells (495.56 ± 144.59 versus 401.59 ± 94.80; P = 0.12; (d)). PBMCs: peripheral blood mononuclear cells; SLE: systemic lupus erythematosus. The expression data of MICB was captured from ArrayExpress Archive database (http://www.ebi.ac.uk/arrayexpress/).
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fig2: Gene differential expression analyses of MICB in immune cell subsets and renal biopsies from SLE patients and controls. (a)–(h) present the MICB expression levels in immune cell subsets and renal biopsy samples from SLE patients and normal donor controls. MICB mRNA expression was significantly or marginally significantly upregulated in SLE B cells (489.80 ± 95.50 versus 352.66 ± 96.13; P = 1.31 × 10−2; (b)), monocytes (1661.14 ± 532.87 versus 1065.38 ± 220.72; P = 4.97 × 10−2; (e)), tubulointerstitial samples (4.33 ± 0.22 versus 4.21 ± 0.16; P = 7.45 × 10−2; (g)), and glomeruli samples (7.92 ± 0.52 versus 6.77 ± 0.23; P = 2.18 × 10−13; (h)). Although with a rather small sample size, a marginally significantly higher expression level of MICB has been observed in monocytes from healthy donors incubated with SLE sera compared to those incubated with autologous serum (1047.50 ± 494.43 versus 300.40 ± 48.88; P = 5.98 × 10−2; (f)), while there was no difference of MICB mRNA expression in PBMC (1577.45 ± 488.74 versus 1610.67 ± 325.23; P = 0.78; (a)), CD3+ T cells (2195.09 ± 865.77 versus 1900.54 ± 715.70; P = 0.35; (c)), and CD4+ T cells (495.56 ± 144.59 versus 401.59 ± 94.80; P = 0.12; (d)). PBMCs: peripheral blood mononuclear cells; SLE: systemic lupus erythematosus. The expression data of MICB was captured from ArrayExpress Archive database (http://www.ebi.ac.uk/arrayexpress/).

Mentions: Using the ArrayExpress Archive database, we further ascertained whether MICB was expressed differently in SLE patients and healthy controls. As was shown in Figure 2, MICB mRNA expression was significantly or marginally significantly upregulated in SLE B cells (489.80 ± 95.50 versus 352.66 ± 96.13; P = 1.31 × 10−2; 7 SLE patients versus 9 controls), monocytes (1661.14 ± 532.87 versus 1065.38 ± 220.72; P = 4.97 × 10−2; 5 SLE patients versus 5 controls), tubulointerstitial samples (4.33 ± 0.22 versus 4.21 ± 0.16; P = 7.45 × 10−2; 32 SLE patients versus 15 controls), and glomeruli samples (7.92 ± 0.52 versus 6.77 ± 0.23; P = 2.18 × 10−13; 32 SLE patients versus 14 controls). Interestingly, although with a rather small sample size, a marginally significantly higher expression level of MICB has been observed in monocytes from healthy donors incubated with SLE sera compared to those incubated with autologous serum (1047.50 ± 494.43 versus 300.40 ± 48.88; P = 5.98 × 10−2; 3 SLE patients versus 3 controls), while there was no difference of MICB mRNA expression in PBMC (1577.45 ± 488.74 versus 1610.67 ± 325.23; P = 0.78; 61 SLE patients versus 20 controls), CD3+ T cells (2195.09 ± 865.77 versus 1900.54 ± 715.70; P = 0.35; 10 SLE patients versus 17 controls), and CD4+ T cells (495.56 ± 144.59 versus 401.59 ± 94.80; P = 0.12; 8 SLE patients versus 10 controls) (Figure 2).


Polymorphism rs3828903 within MICB Is Associated with Susceptibility to Systemic Lupus Erythematosus in a Northern Han Chinese Population.

Zhang YM, Zhou XJ, Cheng FJ, Qi YY, Hou P, Zhao MH, Zhang H - J Immunol Res (2016)

Gene differential expression analyses of MICB in immune cell subsets and renal biopsies from SLE patients and controls. (a)–(h) present the MICB expression levels in immune cell subsets and renal biopsy samples from SLE patients and normal donor controls. MICB mRNA expression was significantly or marginally significantly upregulated in SLE B cells (489.80 ± 95.50 versus 352.66 ± 96.13; P = 1.31 × 10−2; (b)), monocytes (1661.14 ± 532.87 versus 1065.38 ± 220.72; P = 4.97 × 10−2; (e)), tubulointerstitial samples (4.33 ± 0.22 versus 4.21 ± 0.16; P = 7.45 × 10−2; (g)), and glomeruli samples (7.92 ± 0.52 versus 6.77 ± 0.23; P = 2.18 × 10−13; (h)). Although with a rather small sample size, a marginally significantly higher expression level of MICB has been observed in monocytes from healthy donors incubated with SLE sera compared to those incubated with autologous serum (1047.50 ± 494.43 versus 300.40 ± 48.88; P = 5.98 × 10−2; (f)), while there was no difference of MICB mRNA expression in PBMC (1577.45 ± 488.74 versus 1610.67 ± 325.23; P = 0.78; (a)), CD3+ T cells (2195.09 ± 865.77 versus 1900.54 ± 715.70; P = 0.35; (c)), and CD4+ T cells (495.56 ± 144.59 versus 401.59 ± 94.80; P = 0.12; (d)). PBMCs: peripheral blood mononuclear cells; SLE: systemic lupus erythematosus. The expression data of MICB was captured from ArrayExpress Archive database (http://www.ebi.ac.uk/arrayexpress/).
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Related In: Results  -  Collection

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fig2: Gene differential expression analyses of MICB in immune cell subsets and renal biopsies from SLE patients and controls. (a)–(h) present the MICB expression levels in immune cell subsets and renal biopsy samples from SLE patients and normal donor controls. MICB mRNA expression was significantly or marginally significantly upregulated in SLE B cells (489.80 ± 95.50 versus 352.66 ± 96.13; P = 1.31 × 10−2; (b)), monocytes (1661.14 ± 532.87 versus 1065.38 ± 220.72; P = 4.97 × 10−2; (e)), tubulointerstitial samples (4.33 ± 0.22 versus 4.21 ± 0.16; P = 7.45 × 10−2; (g)), and glomeruli samples (7.92 ± 0.52 versus 6.77 ± 0.23; P = 2.18 × 10−13; (h)). Although with a rather small sample size, a marginally significantly higher expression level of MICB has been observed in monocytes from healthy donors incubated with SLE sera compared to those incubated with autologous serum (1047.50 ± 494.43 versus 300.40 ± 48.88; P = 5.98 × 10−2; (f)), while there was no difference of MICB mRNA expression in PBMC (1577.45 ± 488.74 versus 1610.67 ± 325.23; P = 0.78; (a)), CD3+ T cells (2195.09 ± 865.77 versus 1900.54 ± 715.70; P = 0.35; (c)), and CD4+ T cells (495.56 ± 144.59 versus 401.59 ± 94.80; P = 0.12; (d)). PBMCs: peripheral blood mononuclear cells; SLE: systemic lupus erythematosus. The expression data of MICB was captured from ArrayExpress Archive database (http://www.ebi.ac.uk/arrayexpress/).
Mentions: Using the ArrayExpress Archive database, we further ascertained whether MICB was expressed differently in SLE patients and healthy controls. As was shown in Figure 2, MICB mRNA expression was significantly or marginally significantly upregulated in SLE B cells (489.80 ± 95.50 versus 352.66 ± 96.13; P = 1.31 × 10−2; 7 SLE patients versus 9 controls), monocytes (1661.14 ± 532.87 versus 1065.38 ± 220.72; P = 4.97 × 10−2; 5 SLE patients versus 5 controls), tubulointerstitial samples (4.33 ± 0.22 versus 4.21 ± 0.16; P = 7.45 × 10−2; 32 SLE patients versus 15 controls), and glomeruli samples (7.92 ± 0.52 versus 6.77 ± 0.23; P = 2.18 × 10−13; 32 SLE patients versus 14 controls). Interestingly, although with a rather small sample size, a marginally significantly higher expression level of MICB has been observed in monocytes from healthy donors incubated with SLE sera compared to those incubated with autologous serum (1047.50 ± 494.43 versus 300.40 ± 48.88; P = 5.98 × 10−2; 3 SLE patients versus 3 controls), while there was no difference of MICB mRNA expression in PBMC (1577.45 ± 488.74 versus 1610.67 ± 325.23; P = 0.78; 61 SLE patients versus 20 controls), CD3+ T cells (2195.09 ± 865.77 versus 1900.54 ± 715.70; P = 0.35; 10 SLE patients versus 17 controls), and CD4+ T cells (495.56 ± 144.59 versus 401.59 ± 94.80; P = 0.12; 8 SLE patients versus 10 controls) (Figure 2).

Bottom Line: In silico analyses predicted a higher affinity to transcription factors for allele G (risk) and cis-expression quantitative trait loci (cis-eQTL) effects of rs3828903 in multiple tissues (P ranging from 2.79 × 10(-6) to 6.27 × 10(-38)).Furthermore, higher mRNA expressions of MICB were observed in B cells, monocytes, and renal biopsies from SLE patients compared to controls.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Renal Division, Peking University First Hospital, Beijing 100034, China; Peking University Institute of Nephrology, Beijing 100034, China; Key Laboratory of Renal Disease, Ministry of Health of China, Beijing 100034, China; Key Laboratory of Chronic Kidney Disease Prevention and Treatment, Peking University, Ministry of Education, Beijing 100034, China.

ABSTRACT
Objectives. The variant rs3828903 within MICB, a nonclassical MHC class I chain-related gene, was detected to contribute to systemic lupus erythematosus (SLE) in a Caucasian population. This study aimed to investigate the association in a northern Han Chinese population. Methods. We recruited 1077 SLE patients and 793 controls for analysis. rs3828903 was genotyped by TaqMan allele discrimination assay. Using the public databases, its functional annotations and gene differential expression analysis of MICB were evaluated. Results. Significant association between the allele G of rs3828903 and risk susceptibility to SLE was observed after adjusting for sex and age (P = 1.87 × 10(-2)). In silico analyses predicted a higher affinity to transcription factors for allele G (risk) and cis-expression quantitative trait loci (cis-eQTL) effects of rs3828903 in multiple tissues (P ranging from 2.79 × 10(-6) to 6.27 × 10(-38)). Furthermore, higher mRNA expressions of MICB were observed in B cells, monocytes, and renal biopsies from SLE patients compared to controls. Conclusion. An association between rs3828903 and susceptibility to SLE has been detected in a Chinese population. This together with the functional annotations of rs3828903 converts MICB into a main candidate in the pathogenesis of SLE.

No MeSH data available.


Related in: MedlinePlus