Association of RIP2 gene polymorphisms and systemic lupus erythematosus in a Chinese population.

The aim of this study was to investigate the association of receptor interacting protein 2 (RIP2) single-nucleotide polymorphisms (SNPs) with susceptibility to systemic lupus erythematosus (SLE) in a Chinese population. A case-control study was performed on the SNPs rs16900617 and rs16900627 in 590 Chinese SLE patients and 660 healthy controls. These SNPs were typed by TaqMan allele discrimination assays. We found a significant association of rs16900617 G allele [odds ratio (OR) = 0.54, 95% confidence interval (CI) 0.41-0.72] and rs16900627 G allele (OR = 1.28, 95% CI 1.04-1.58) with SLE. Significant differences in genotype frequency distribution were also found in SLE and control individuals (rs16900617: AG versus AA, OR = 0.59, 95% CI 0.44-0.81; GG versus AA, OR = 0.08, 95% CI 0.01-0.65; AG + GG versus AA, OR = 0.55, 95% CI 0.41-0.75; rs16900627: AG versus AA, OR = 1.51, 95% CI 1.17-1.93; AG + GG versus AA, OR = 1.43, 95% CI 1.13-1.82). Analysis of the haplotypes revealed that two haplotypes of AG and GA were also significantly associated with SLE (OR = 1.37, 95% CI 1.11-1.70; OR = 0.60, 95% CI 0.45-0.79). Our findings suggest that the RIP2 gene polymorphisms may be associated with susceptibility to SLE in the Chinese population.

[1]  C. O'Morain,et al.  RIP2 polymorphisms in inflammatory bowel diseases. , 2011, Inflammatory Bowel Diseases.

[2]  S. Zheng,et al.  Involvement of CD226+ NK Cells in Immunopathogenesis of Systemic Lupus Erythematosus , 2011, The Journal of Immunology.

[3]  Maureen A. McGargill,et al.  Signaling via the RIP2 adaptor protein in central nervous system-infiltrating dendritic cells promotes inflammation and autoimmunity. , 2011, Immunity.

[4]  A. Farris,et al.  Targeting Toll-Like Receptors for Treatment of SLE , 2010, Mediators of inflammation.

[5]  Ying Wang,et al.  Genomewide association study of leprosy. , 2009, The New England journal of medicine.

[6]  P. Scacheri,et al.  ITCH K63-Ubiquitinates the NOD2 Binding Protein, RIP2, to Influence Inflammatory Signaling Pathways , 2009, Current Biology.

[7]  L. Stronati,et al.  Activation of NOD2‐mediated intestinal pathway in a pediatric population with Crohn's disease , 2009, Inflammatory bowel diseases.

[8]  S. Su,et al.  The critical role of Toll-like receptor signaling pathways in the induction and progression of autoimmune diseases. , 2009, Current molecular medicine.

[9]  S. Navarra,et al.  Lupus in the developing world--is it any different? , 2008, Best practice & research. Clinical rheumatology.

[10]  T. Mak,et al.  RIP2 contributes to Nod signaling but is not essential for T cell proliferation, T helper differentiation or TLR responses , 2008, European journal of immunology.

[11]  Grace Y Chen,et al.  Intracellular NOD‐like receptors in innate immunity, infection and disease , 2007, Cellular microbiology.

[12]  Christine E. Becker,et al.  Inflammasomes in inflammatory disorders: the role of TLRs and their interactions with NLRs , 2007, Seminars in Immunopathology.

[13]  R. Ulevitch,et al.  SGT1 is essential for Nod1 activation , 2007, Proceedings of the National Academy of Sciences.

[14]  G. Núñez,et al.  RICK/RIP2 Mediates Innate Immune Responses Induced through Nod1 and Nod2 but Not TLRs1 , 2007, The Journal of Immunology.

[15]  D. Goeddel,et al.  NF-κB-Inducing Kinase Regulates Selected Gene Expression in the Nod2 Signaling Pathway , 2006, Infection and Immunity.

[16]  Yusuke Nakamura,et al.  Association of the RIP2 gene with childhood atopic asthma. , 2006, Allergology international : official journal of the Japanese Society of Allergology.

[17]  S. Girardin,et al.  How Toll-like receptors and Nod-like receptors contribute to innate immunity in mammals , 2005, Journal of endotoxin research.

[18]  P. Malfertheiner,et al.  Inhibition of RICK/Nuclear Factor-κB and p38 Signaling Attenuates the Inflammatory Response in a Murine Model of Crohn Disease* , 2005, Journal of Biological Chemistry.

[19]  Lin He,et al.  SHEsis, a powerful software platform for analyses of linkage disequilibrium, haplotype construction, and genetic association at polymorphism loci , 2005, Cell Research.

[20]  G. Cheng,et al.  Rip2: A Key Molecule that Regulates both Innate and Acquired Immunity , 2005 .

[21]  L. Cantley,et al.  The Crohn's Disease Protein, NOD2, Requires RIP2 in Order to Induce Ubiquitinylation of a Novel Site on NEMO , 2004, Current Biology.

[22]  D. Philpott,et al.  Peptidoglycan Molecular Requirements Allowing Detection by Nod1 and Nod2* , 2003, Journal of Biological Chemistry.

[23]  C. Janeway,et al.  RICK/Rip2/CARDIAK mediates signalling for receptors of the innate and adaptive immune systems , 2002, Nature.

[24]  G. Cheng,et al.  Involvement of receptor-interacting protein 2 in innate and adaptive immune responses , 2002, Nature.

[25]  T. Behrens,et al.  Delineating the genetic basis of systemic lupus erythematosus. , 2001, Immunity.

[26]  J. Bertin,et al.  CARD4/Nod1 mediates NF‐κB and JNK activation by invasive Shigella flexneri , 2001 .

[27]  F. Martinon,et al.  Identification of CARDIAK, a RIP-like kinase that associates with caspase-1 , 1998, Current Biology.

[28]  V. Dixit,et al.  RIP2 Is a Novel NF-κB-activating and Cell Death-inducing Kinase* , 1998, The Journal of Biological Chemistry.

[29]  L. del Peso,et al.  RICK, a Novel Protein Kinase Containing a Caspase Recruitment Domain, Interacts with CLARP and Regulates CD95-mediated Apoptosis* , 1998, The Journal of Biological Chemistry.

[30]  J. Buolamwini.  Nucleoside Transport Inhibitors: Structure-Activity Relationships and Potential Therapeutic Applications , 1997, Current Medicinal Chemistry.

[31]  M. Hochberg,et al.  Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. , 1997, Arthritis and rheumatism.

[32]  E. Hess.  Environmental lupus syndromes. , 1995, British journal of rheumatology.

[33]  J F Fries,et al.  The 1982 revised criteria for the classification of systemic lupus erythematosus. , 1982, Arthritis and rheumatism.