Skip to main content
Erschienen in: International Journal of Colorectal Disease 9/2011

01.09.2011 | Original Article

Interaction between CTLA4 gene and IBD5 locus in Hungarian Crohn’s disease patients

verfasst von: Veronika Csöngei, Luca Járomi, Enikő Sáfrány, Csilla Sipeky, Lili Magyari, Noémi Polgár, Judit Bene, Patrícia Sarlós, Lilla Lakner, Eszter Baricza, Melinda Szabó, Gábor Rappai, Béla Melegh

Erschienen in: International Journal of Colorectal Disease | Ausgabe 9/2011

Einloggen, um Zugang zu erhalten

Abstract

Backgrounds and aims

The IGR2198a_1 and IGR2096a_1 variants of the IBD5 region were found to be associated with Crohn’s disease (CD) in the Hungarian population, while IGR2230a_1 does not seem to confer risk for the disease. In the present study, our aim was to investigate the statistical interaction of these three IBD5 polymorphisms with the +49 A/G substitution within the cytotoxic T lymphocyte antigen-4 (CTLA4) gene, detected previously as neutral gene variant in Hungarian IBD patients.

Methods

A total of 305 unrelated subjects with CD and 310 healthy controls were genotyped with PCR-RFLP methods.

Results

In contrast with single gene effects, after genotype stratification, the IGR2198a_1 C and IGR2096a_1 T variants were found to confer susceptibility only in subjects with CTLA4 +49 AA genotype (P = 0.008; OR = 1.86 and P = 0.016; OR = 1.74, respectively), for IGR2230a_1 no such effect on disease risk could be demonstrated.

Conclusion

Analysis of specific genotype combinations unfolded a possible association between the CTLA4 +49 A/G substitution and two of the observed IBD5 variants with respect to disease risk.
Literatur
1.
Zurück zum Zitat Moore JH (2003) The ubiquitous nature of epistasis in determining susceptibility to common human diseases. Hum Hered 56:73–82PubMedCrossRef Moore JH (2003) The ubiquitous nature of epistasis in determining susceptibility to common human diseases. Hum Hered 56:73–82PubMedCrossRef
2.
Zurück zum Zitat Cordell HJ (2002) Epistasis: what it means, what it doesn’t mean, and statistical methods to detect it in humans. Hum Mol Genet 11:2463–2468PubMedCrossRef Cordell HJ (2002) Epistasis: what it means, what it doesn’t mean, and statistical methods to detect it in humans. Hum Mol Genet 11:2463–2468PubMedCrossRef
3.
Zurück zum Zitat Magyari L, Farago B, Bene J et al (2007) No association of the cytotoxic T-lymphocyte associated gene CTLA4 +49A/G polymorphisms with Crohn’s disease and ulcerative colitis in Hungarian population samples. World J Gastroenterol 13:2205–2208PubMed Magyari L, Farago B, Bene J et al (2007) No association of the cytotoxic T-lymphocyte associated gene CTLA4 +49A/G polymorphisms with Crohn’s disease and ulcerative colitis in Hungarian population samples. World J Gastroenterol 13:2205–2208PubMed
4.
Zurück zum Zitat Talian G, Lakner L, Bene J et al (2009) Plasma carnitine ester profiles in Crohn’s disease and ulcerative colitis patients with different IGR2230a_1 genotypes. Int J Immunogenet 36:329–335PubMedCrossRef Talian G, Lakner L, Bene J et al (2009) Plasma carnitine ester profiles in Crohn’s disease and ulcerative colitis patients with different IGR2230a_1 genotypes. Int J Immunogenet 36:329–335PubMedCrossRef
5.
Zurück zum Zitat Lakner L, Csongei V, Sarlos P et al (2009) IGR2096a_1 T and IGR2198a_1 C alleles on IBD5 locus of chromosome 5q31 region confer risk for Crohn’s disease in Hungarian patients. Int J Colorectal Dis 24:503–507PubMedCrossRef Lakner L, Csongei V, Sarlos P et al (2009) IGR2096a_1 T and IGR2198a_1 C alleles on IBD5 locus of chromosome 5q31 region confer risk for Crohn’s disease in Hungarian patients. Int J Colorectal Dis 24:503–507PubMedCrossRef
6.
Zurück zum Zitat Culverhouse R, Suarez BK, Lin J, Reich T (2002) A perspective on epistasis: limits of models displaying no main effect. Am J Hum Genet 70:461–471PubMedCrossRef Culverhouse R, Suarez BK, Lin J, Reich T (2002) A perspective on epistasis: limits of models displaying no main effect. Am J Hum Genet 70:461–471PubMedCrossRef
7.
Zurück zum Zitat Hampe J, Franke A, Rosenstiel P et al (2007) A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nat Genet 39:207–211PubMedCrossRef Hampe J, Franke A, Rosenstiel P et al (2007) A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. Nat Genet 39:207–211PubMedCrossRef
8.
Zurück zum Zitat Safrany E, Melegh B (2009) Functional variants of the interleukin-23 receptor gene in non-gastrointestinal autoimmune diseases. Curr Med Chem 16:3766–3774PubMedCrossRef Safrany E, Melegh B (2009) Functional variants of the interleukin-23 receptor gene in non-gastrointestinal autoimmune diseases. Curr Med Chem 16:3766–3774PubMedCrossRef
9.
Zurück zum Zitat Farago B, Magyari L, Safrany E et al (2008) Functional variants of interleukin-23 receptor gene confer risk for rheumatoid arthritis but not for systemic sclerosis. Ann Rheum Dis 67:248–250PubMedCrossRef Farago B, Magyari L, Safrany E et al (2008) Functional variants of interleukin-23 receptor gene confer risk for rheumatoid arthritis but not for systemic sclerosis. Ann Rheum Dis 67:248–250PubMedCrossRef
10.
Zurück zum Zitat Cummings JR, Cooney R, Pathan S et al (2007) Confirmation of the role of ATG16L1 as a Crohn’s disease susceptibility gene. Inflamm Bowel Dis 13:941–946PubMedCrossRef Cummings JR, Cooney R, Pathan S et al (2007) Confirmation of the role of ATG16L1 as a Crohn’s disease susceptibility gene. Inflamm Bowel Dis 13:941–946PubMedCrossRef
11.
Zurück zum Zitat Prescott NJ, Fisher SA, Franke A et al (2007) A nonsynonymous SNP in ATG16L1 predisposes to ileal Crohn’s disease and is independent of CARD15 and IBD5. Gastroenterology 132:1665–1671PubMedCrossRef Prescott NJ, Fisher SA, Franke A et al (2007) A nonsynonymous SNP in ATG16L1 predisposes to ileal Crohn’s disease and is independent of CARD15 and IBD5. Gastroenterology 132:1665–1671PubMedCrossRef
12.
Zurück zum Zitat Glas J, Konrad A, Schmechel S et al (2008) The ATG16L1 gene variants rs2241879 and rs2241880 (T300A) are strongly associated with susceptibility to Crohn’s disease in the German population. Am J Gastroenterol 103:682–691PubMedCrossRef Glas J, Konrad A, Schmechel S et al (2008) The ATG16L1 gene variants rs2241879 and rs2241880 (T300A) are strongly associated with susceptibility to Crohn’s disease in the German population. Am J Gastroenterol 103:682–691PubMedCrossRef
13.
Zurück zum Zitat Latiano A, Palmieri O, Valvano MR et al (2008) Replication of interleukin 23 receptor and autophagy-related 16-like 1 association in adult- and pediatric-onset inflammatory bowel disease in Italy. World J Gastroenterol 14:4643–4651PubMedCrossRef Latiano A, Palmieri O, Valvano MR et al (2008) Replication of interleukin 23 receptor and autophagy-related 16-like 1 association in adult- and pediatric-onset inflammatory bowel disease in Italy. World J Gastroenterol 14:4643–4651PubMedCrossRef
14.
Zurück zum Zitat Roberts RL, Gearry RB, Hollis-Moffatt JE et al (2007) IL23R R381Q and ATG16L1 T300A are strongly associated with Crohn’s disease in a study of New Zealand Caucasians with inflammatory bowel disease. Am J Gastroenterol 102:2754–2761PubMedCrossRef Roberts RL, Gearry RB, Hollis-Moffatt JE et al (2007) IL23R R381Q and ATG16L1 T300A are strongly associated with Crohn’s disease in a study of New Zealand Caucasians with inflammatory bowel disease. Am J Gastroenterol 102:2754–2761PubMedCrossRef
15.
Zurück zum Zitat Glas J, Seiderer J, Wetzke M et al (2007) rs1004819 is the main disease-associated IL23R variant in German Crohn’s disease patients: combined analysis of IL23R, CARD15, and OCTN1/2 variants. PLoS ONE 2:e819PubMedCrossRef Glas J, Seiderer J, Wetzke M et al (2007) rs1004819 is the main disease-associated IL23R variant in German Crohn’s disease patients: combined analysis of IL23R, CARD15, and OCTN1/2 variants. PLoS ONE 2:e819PubMedCrossRef
16.
Zurück zum Zitat Latiano A, Palmieri O, Valvano RM et al (2006) Contribution of IBD5 locus to clinical features of IBD patients. Am J Gastroenterol 101:318–325PubMedCrossRef Latiano A, Palmieri O, Valvano RM et al (2006) Contribution of IBD5 locus to clinical features of IBD patients. Am J Gastroenterol 101:318–325PubMedCrossRef
17.
Zurück zum Zitat Weersma RK, Stokkers PC, van Bodegraven AA et al (2009) Molecular prediction of disease risk and severity in a large Dutch Crohn’s disease cohort. Gut 58:388–395PubMedCrossRef Weersma RK, Stokkers PC, van Bodegraven AA et al (2009) Molecular prediction of disease risk and severity in a large Dutch Crohn’s disease cohort. Gut 58:388–395PubMedCrossRef
18.
Zurück zum Zitat Csongei V, Jaromi L, Safrany E et al (2010) Interaction of the major inflammatory bowel disease susceptibility alleles in Crohn’s disease patients. World J Gastroenterol 16:176–183PubMedCrossRef Csongei V, Jaromi L, Safrany E et al (2010) Interaction of the major inflammatory bowel disease susceptibility alleles in Crohn’s disease patients. World J Gastroenterol 16:176–183PubMedCrossRef
19.
Zurück zum Zitat Okazaki T, Wang MH, Rawsthorne P et al (2008) Contributions of IBD5, IL23R, ATG16L1, and NOD2 to Crohn’s disease risk in a population-based case-control study: evidence of gene-gene interactions. Inflamm Bowel Dis 14:1528–1541PubMedCrossRef Okazaki T, Wang MH, Rawsthorne P et al (2008) Contributions of IBD5, IL23R, ATG16L1, and NOD2 to Crohn’s disease risk in a population-based case-control study: evidence of gene-gene interactions. Inflamm Bowel Dis 14:1528–1541PubMedCrossRef
20.
Zurück zum Zitat Petermann I, Huebner C, Browning BL et al (2009) Interactions among genes influencing bacterial recognition increase IBD risk in a population-based New Zealand cohort. Hum Immunol 70:440–446PubMedCrossRef Petermann I, Huebner C, Browning BL et al (2009) Interactions among genes influencing bacterial recognition increase IBD risk in a population-based New Zealand cohort. Hum Immunol 70:440–446PubMedCrossRef
21.
Zurück zum Zitat McGovern DP, Rotter JI, Mei L et al (2009) Genetic epistasis of IL23/IL17 pathway genes in Crohn’s disease. Inflamm Bowel Dis 15:883–889PubMedCrossRef McGovern DP, Rotter JI, Mei L et al (2009) Genetic epistasis of IL23/IL17 pathway genes in Crohn’s disease. Inflamm Bowel Dis 15:883–889PubMedCrossRef
22.
Zurück zum Zitat Marquez A, Varade J, Robledo G et al (2009) Specific association of a CLEC16A/KIAA0350 polymorphism with NOD2/CARD15(−) Crohn’s disease patients. Eur J Hum Genet 17:1304–1308PubMedCrossRef Marquez A, Varade J, Robledo G et al (2009) Specific association of a CLEC16A/KIAA0350 polymorphism with NOD2/CARD15(−) Crohn’s disease patients. Eur J Hum Genet 17:1304–1308PubMedCrossRef
23.
Zurück zum Zitat Machida H, Tsukamoto K, Wen CY et al (2005) Association of polymorphic alleles of CTLA4 with inflammatory bowel disease in the Japanese. World J Gastroenterol 11:4188–4193PubMed Machida H, Tsukamoto K, Wen CY et al (2005) Association of polymorphic alleles of CTLA4 with inflammatory bowel disease in the Japanese. World J Gastroenterol 11:4188–4193PubMed
24.
Zurück zum Zitat Ben Alaya W, Sfar I, Aouadi H et al (2009) Association between CTLA-4 gene promoter (49 A/G) in exon 1 polymorphisms and inflammatory bowel disease in the Tunisian population. Saudi J Gastroenterol 15:29–34PubMedCrossRef Ben Alaya W, Sfar I, Aouadi H et al (2009) Association between CTLA-4 gene promoter (49 A/G) in exon 1 polymorphisms and inflammatory bowel disease in the Tunisian population. Saudi J Gastroenterol 15:29–34PubMedCrossRef
25.
Zurück zum Zitat Xia B, Crusius JB, Wu J, Zwiers A, van Bodegraven AA, Pena AS (2002) CTLA4 gene polymorphisms in Dutch and Chinese patients with inflammatory bowel disease. Scand J Gastroenterol 37:1296–1300PubMedCrossRef Xia B, Crusius JB, Wu J, Zwiers A, van Bodegraven AA, Pena AS (2002) CTLA4 gene polymorphisms in Dutch and Chinese patients with inflammatory bowel disease. Scand J Gastroenterol 37:1296–1300PubMedCrossRef
26.
Zurück zum Zitat Hou W, Xia B, Yuan A, Li J, Yang Z, Mao L (2005) CTLA-4 gene polymorphisms in Chinese patients with ulcerative colitis. Inflamm Bowel Dis 11:653–656PubMedCrossRef Hou W, Xia B, Yuan A, Li J, Yang Z, Mao L (2005) CTLA-4 gene polymorphisms in Chinese patients with ulcerative colitis. Inflamm Bowel Dis 11:653–656PubMedCrossRef
27.
Zurück zum Zitat Lankarani KB, Karbasi A, Kalantari T et al (2006) Analysis of cytotoxic T lymphocyte associated antigen 4 gene polymorphisms in patients with ulcerative colitis. J Gastroenterol Hepatol 21:449–453PubMedCrossRef Lankarani KB, Karbasi A, Kalantari T et al (2006) Analysis of cytotoxic T lymphocyte associated antigen 4 gene polymorphisms in patients with ulcerative colitis. J Gastroenterol Hepatol 21:449–453PubMedCrossRef
28.
Zurück zum Zitat Hradsky O, Dusatkova P, Lenicek M et al (2010) The CTLA4 variants may interact with the IL23R- and NOD2-conferred risk in the development of Crohn’s disease. BMC Med Genet 11:91PubMedCrossRef Hradsky O, Dusatkova P, Lenicek M et al (2010) The CTLA4 variants may interact with the IL23R- and NOD2-conferred risk in the development of Crohn’s disease. BMC Med Genet 11:91PubMedCrossRef
29.
Zurück zum Zitat Abe T, Takino H, Yamasaki H et al (1999) CTLA4 gene polymorphism correlates with the mode of onset and presence of ICA512 Ab in Japanese type 1 diabetes. Diabetes Res Clin Pract 46:169–175PubMedCrossRef Abe T, Takino H, Yamasaki H et al (1999) CTLA4 gene polymorphism correlates with the mode of onset and presence of ICA512 Ab in Japanese type 1 diabetes. Diabetes Res Clin Pract 46:169–175PubMedCrossRef
30.
Zurück zum Zitat Cinek O, Drevinek P, Sumnik Z et al (2002) The CTLA4 +49 A/G dimorphism is not associated with type 1 diabetes in Czech children. Eur J Immunogenet 29:219–222PubMedCrossRef Cinek O, Drevinek P, Sumnik Z et al (2002) The CTLA4 +49 A/G dimorphism is not associated with type 1 diabetes in Czech children. Eur J Immunogenet 29:219–222PubMedCrossRef
31.
Zurück zum Zitat Donner H, Rau H, Walfish PG et al (1997) CTLA4 alanine-17 confers genetic susceptibility to Graves’ disease and to type 1 diabetes mellitus. J Clin Endocrinol Metab 82:143–146PubMedCrossRef Donner H, Rau H, Walfish PG et al (1997) CTLA4 alanine-17 confers genetic susceptibility to Graves’ disease and to type 1 diabetes mellitus. J Clin Endocrinol Metab 82:143–146PubMedCrossRef
32.
Zurück zum Zitat Lee YJ, Huang FY, Lo FS et al (2000) Association of CTLA4 gene A-G polymorphism with type 1 diabetes in Chinese children. Clin Endocrinol 52:153–157CrossRef Lee YJ, Huang FY, Lo FS et al (2000) Association of CTLA4 gene A-G polymorphism with type 1 diabetes in Chinese children. Clin Endocrinol 52:153–157CrossRef
33.
Zurück zum Zitat Nistico L, Buzzetti R, Pritchard LE et al (1996) The CTLA-4 gene region of chromosome 2q33 is linked to, and associated with, type 1 diabetes. Belgian Diabetes Registry. Hum Mol Genet 5:1075–1080PubMedCrossRef Nistico L, Buzzetti R, Pritchard LE et al (1996) The CTLA-4 gene region of chromosome 2q33 is linked to, and associated with, type 1 diabetes. Belgian Diabetes Registry. Hum Mol Genet 5:1075–1080PubMedCrossRef
34.
Zurück zum Zitat Osei-Hyiaman D, Hou L, Zhiyin R et al (2001) Association of a novel point mutation (C159G) of the CTLA4 gene with type 1 diabetes in West Africans but not in Chinese. Diabetes 50:2169–2171PubMedCrossRef Osei-Hyiaman D, Hou L, Zhiyin R et al (2001) Association of a novel point mutation (C159G) of the CTLA4 gene with type 1 diabetes in West Africans but not in Chinese. Diabetes 50:2169–2171PubMedCrossRef
35.
Zurück zum Zitat Zalloua PA, Abchee A, Shbaklo H et al (2004) Patients with early onset of type 1 diabetes have significantly higher GG genotype at position 49 of the CTLA4 gene. Hum Immunol 65:719–724PubMedCrossRef Zalloua PA, Abchee A, Shbaklo H et al (2004) Patients with early onset of type 1 diabetes have significantly higher GG genotype at position 49 of the CTLA4 gene. Hum Immunol 65:719–724PubMedCrossRef
36.
Zurück zum Zitat Lemos MC, Coutinho E, Gomes L et al (2009) The CTLA4 +49 A/G polymorphism is not associated with susceptibility to type 1 diabetes mellitus in the Portuguese population. Int J Immunogenet 36:193–195PubMedCrossRef Lemos MC, Coutinho E, Gomes L et al (2009) The CTLA4 +49 A/G polymorphism is not associated with susceptibility to type 1 diabetes mellitus in the Portuguese population. Int J Immunogenet 36:193–195PubMedCrossRef
37.
Zurück zum Zitat Borhani HA, Ghahramani S, Azarpira N, Pourjafar M, Nikseresht AR (2008) Cytotoxic T lymphocyte associated antigen-4 exon 1 A/G polymorphism in Iranian patients with multiple sclerosis. Eur J Neurol 15:862–864CrossRef Borhani HA, Ghahramani S, Azarpira N, Pourjafar M, Nikseresht AR (2008) Cytotoxic T lymphocyte associated antigen-4 exon 1 A/G polymorphism in Iranian patients with multiple sclerosis. Eur J Neurol 15:862–864CrossRef
38.
Zurück zum Zitat Heggarty S, Suppiah V, Silversides J et al (2007) CTLA4 gene polymorphisms and multiple sclerosis in Northern Ireland. J Neuroimmunol 187:187–191PubMedCrossRef Heggarty S, Suppiah V, Silversides J et al (2007) CTLA4 gene polymorphisms and multiple sclerosis in Northern Ireland. J Neuroimmunol 187:187–191PubMedCrossRef
39.
Zurück zum Zitat Yousefipour G, Erfani N, Momtahan M, Moghaddasi H, Ghaderi A (2009) CTLA4 exon 1 and promoter polymorphisms in patients with multiple sclerosis. Acta Neurol Scand 120:424–429PubMedCrossRef Yousefipour G, Erfani N, Momtahan M, Moghaddasi H, Ghaderi A (2009) CTLA4 exon 1 and promoter polymorphisms in patients with multiple sclerosis. Acta Neurol Scand 120:424–429PubMedCrossRef
40.
Zurück zum Zitat Bilinska M, Frydecka I, Noga L et al (2004) Progression of multiple sclerosis is associated with exon 1 CTLA-4 gene polymorphism. Acta Neurol Scand 110:67–71PubMedCrossRef Bilinska M, Frydecka I, Noga L et al (2004) Progression of multiple sclerosis is associated with exon 1 CTLA-4 gene polymorphism. Acta Neurol Scand 110:67–71PubMedCrossRef
41.
Zurück zum Zitat Heward JM, Allahabadia A, Armitage M et al (1999) The development of Graves’ disease and the CTLA-4 gene on chromosome 2q33. J Clin Endocrinol Metab 84:2398–2401PubMedCrossRef Heward JM, Allahabadia A, Armitage M et al (1999) The development of Graves’ disease and the CTLA-4 gene on chromosome 2q33. J Clin Endocrinol Metab 84:2398–2401PubMedCrossRef
42.
Zurück zum Zitat Kinjo Y, Takasu N, Komiya I et al (2002) Remission of Graves’ hyperthyroidism and A/G polymorphism at position 49 in exon 1 of cytotoxic T lymphocyte-associated molecule-4 gene. J Clin Endocrinol Metab 87:2593–2596PubMedCrossRef Kinjo Y, Takasu N, Komiya I et al (2002) Remission of Graves’ hyperthyroidism and A/G polymorphism at position 49 in exon 1 of cytotoxic T lymphocyte-associated molecule-4 gene. J Clin Endocrinol Metab 87:2593–2596PubMedCrossRef
43.
Zurück zum Zitat Kouki T, Gardine CA, Yanagawa T, DeGroot LJ (2002) Relation of three polymorphisms of the CTLA-4 gene in patients with Graves’ disease. J Endocrinol Investig 25:208–213 Kouki T, Gardine CA, Yanagawa T, DeGroot LJ (2002) Relation of three polymorphisms of the CTLA-4 gene in patients with Graves’ disease. J Endocrinol Investig 25:208–213
44.
Zurück zum Zitat Ueda H, Howson JM, Esposito L et al (2003) Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease. Nature 423:506–511PubMedCrossRef Ueda H, Howson JM, Esposito L et al (2003) Association of the T-cell regulatory gene CTLA4 with susceptibility to autoimmune disease. Nature 423:506–511PubMedCrossRef
45.
Zurück zum Zitat Wang PW, Liu RT, Juo SH et al (2004) Cytotoxic T lymphocyte-associated molecule-4 polymorphism and relapse of Graves’ hyperthyroidism after antithyroid withdrawal. J Clin Endocrinol Metab 89:169–173PubMedCrossRef Wang PW, Liu RT, Juo SH et al (2004) Cytotoxic T lymphocyte-associated molecule-4 polymorphism and relapse of Graves’ hyperthyroidism after antithyroid withdrawal. J Clin Endocrinol Metab 89:169–173PubMedCrossRef
46.
Zurück zum Zitat Donner H, Braun J, Seidl C et al (1997) Codon 17 polymorphism of the cytotoxic T lymphocyte antigen 4 gene in Hashimoto’s thyroiditis and Addison’s disease. J Clin Endocrinol Metab 82:4130–4132PubMedCrossRef Donner H, Braun J, Seidl C et al (1997) Codon 17 polymorphism of the cytotoxic T lymphocyte antigen 4 gene in Hashimoto’s thyroiditis and Addison’s disease. J Clin Endocrinol Metab 82:4130–4132PubMedCrossRef
47.
Zurück zum Zitat Gonzalez-Escribano MF, Rodriguez R, Valenzuela A, Garcia A, Garcia-Lozano JR, Nunez-Roldan A (1999) CTLA4 polymorphisms in Spanish patients with rheumatoid arthritis. Tissue Antigens 53:296–300PubMedCrossRef Gonzalez-Escribano MF, Rodriguez R, Valenzuela A, Garcia A, Garcia-Lozano JR, Nunez-Roldan A (1999) CTLA4 polymorphisms in Spanish patients with rheumatoid arthritis. Tissue Antigens 53:296–300PubMedCrossRef
48.
Zurück zum Zitat Lee CS, Lee YJ, Liu HF et al (2003) Association of CTLA4 gene A-G polymorphism with rheumatoid arthritis in Chinese. Clin Rheumatol 22:221–224PubMedCrossRef Lee CS, Lee YJ, Liu HF et al (2003) Association of CTLA4 gene A-G polymorphism with rheumatoid arthritis in Chinese. Clin Rheumatol 22:221–224PubMedCrossRef
49.
Zurück zum Zitat Barreto M, Santos E, Ferreira R et al (2004) Evidence for CTLA4 as a susceptibility gene for systemic lupus erythematosus. Eur J Hum Genet 12:620–626PubMedCrossRef Barreto M, Santos E, Ferreira R et al (2004) Evidence for CTLA4 as a susceptibility gene for systemic lupus erythematosus. Eur J Hum Genet 12:620–626PubMedCrossRef
50.
Zurück zum Zitat Djilali-Saiah I, Schmitz J, Harfouch-Hammoud E, Mougenot JF, Bach JF, Caillat-Zucman S (1998) CTLA-4 gene polymorphism is associated with predisposition to coeliac disease. Gut 43:187–189PubMedCrossRef Djilali-Saiah I, Schmitz J, Harfouch-Hammoud E, Mougenot JF, Bach JF, Caillat-Zucman S (1998) CTLA-4 gene polymorphism is associated with predisposition to coeliac disease. Gut 43:187–189PubMedCrossRef
51.
Zurück zum Zitat Naluai AT, Nilsson S, Samuelsson L et al (2000) The CTLA4/CD28 gene region on chromosome 2q33 confers susceptibility to celiac disease in a way possibly distinct from that of type 1 diabetes and other chronic inflammatory disorders. Tissue Antigens 56:350–355PubMedCrossRef Naluai AT, Nilsson S, Samuelsson L et al (2000) The CTLA4/CD28 gene region on chromosome 2q33 confers susceptibility to celiac disease in a way possibly distinct from that of type 1 diabetes and other chronic inflammatory disorders. Tissue Antigens 56:350–355PubMedCrossRef
52.
Zurück zum Zitat King AL, Moodie SJ, Fraser JS et al (2003) Coeliac disease: investigation of proposed causal variants in the CTLA4 gene region. Eur J Immunogenet 30:427–432PubMedCrossRef King AL, Moodie SJ, Fraser JS et al (2003) Coeliac disease: investigation of proposed causal variants in the CTLA4 gene region. Eur J Immunogenet 30:427–432PubMedCrossRef
53.
Zurück zum Zitat Martin-Pagola A, Perez dN, Vitoria JC et al (2003) No association of CTLA4 gene with celiac disease in the Basque population. J Pediatr Gastroenterol Nutr 37:142–145PubMedCrossRef Martin-Pagola A, Perez dN, Vitoria JC et al (2003) No association of CTLA4 gene with celiac disease in the Basque population. J Pediatr Gastroenterol Nutr 37:142–145PubMedCrossRef
54.
Zurück zum Zitat Popat S, Hearle N, Wixey J et al (2002) Analysis of the CTLA4 gene in Swedish coeliac disease patients. Scand J Gastroenterol 37:28–31PubMedCrossRef Popat S, Hearle N, Wixey J et al (2002) Analysis of the CTLA4 gene in Swedish coeliac disease patients. Scand J Gastroenterol 37:28–31PubMedCrossRef
55.
Zurück zum Zitat Popat S, Hearle N, Hogberg L et al (2002) Variation in the CTLA4/CD28 gene region confers an increased risk of coeliac disease. Ann Hum Genet 66:125–137PubMedCrossRef Popat S, Hearle N, Hogberg L et al (2002) Variation in the CTLA4/CD28 gene region confers an increased risk of coeliac disease. Ann Hum Genet 66:125–137PubMedCrossRef
56.
Zurück zum Zitat Mora B, Bonamico M, Indovina P et al (2003) CTLA-4 +49 A/G dimorphism in Italian patients with celiac disease. Hum Immunol 64:297–301PubMedCrossRef Mora B, Bonamico M, Indovina P et al (2003) CTLA-4 +49 A/G dimorphism in Italian patients with celiac disease. Hum Immunol 64:297–301PubMedCrossRef
57.
Zurück zum Zitat Gudjonsdottir AH, Nilsson S, Naluai AT et al (2009) Association between genotypes and phenotypes in coeliac disease. J Pediatr Gastroenterol Nutr 49:165–169PubMedCrossRef Gudjonsdottir AH, Nilsson S, Naluai AT et al (2009) Association between genotypes and phenotypes in coeliac disease. J Pediatr Gastroenterol Nutr 49:165–169PubMedCrossRef
58.
Zurück zum Zitat Suppiah V, Alloza I, Heggarty S et al (2005) The CTLA4 +49 A/G*G-CT60*G haplotype is associated with susceptibility to multiple sclerosis in Flanders. J Neuroimmunol 164:148–153PubMedCrossRef Suppiah V, Alloza I, Heggarty S et al (2005) The CTLA4 +49 A/G*G-CT60*G haplotype is associated with susceptibility to multiple sclerosis in Flanders. J Neuroimmunol 164:148–153PubMedCrossRef
59.
Zurück zum Zitat Suppiah V, O'Doherty C, Heggarty S, Patterson CC, Rooney M, Vandenbroeck K (2006) The CTLA4+49A/G and CT60 polymorphisms and chronic inflammatory arthropathies in Northern Ireland. Exp Mol Pathol 80:141–146PubMedCrossRef Suppiah V, O'Doherty C, Heggarty S, Patterson CC, Rooney M, Vandenbroeck K (2006) The CTLA4+49A/G and CT60 polymorphisms and chronic inflammatory arthropathies in Northern Ireland. Exp Mol Pathol 80:141–146PubMedCrossRef
60.
Zurück zum Zitat Downie-Doyle S, Bayat N, Rischmueller M, Lester S (2006) Influence of CTLA4 haplotypes on susceptibility and some extraglandular manifestations in primary Sjogren’s syndrome. Arthritis Rheum 54:2434–2440PubMedCrossRef Downie-Doyle S, Bayat N, Rischmueller M, Lester S (2006) Influence of CTLA4 haplotypes on susceptibility and some extraglandular manifestations in primary Sjogren’s syndrome. Arthritis Rheum 54:2434–2440PubMedCrossRef
61.
Zurück zum Zitat Hunt KA, McGovern DP, Kumar PJ et al (2005) A common CTLA4 haplotype associated with coeliac disease. Eur J Hum Genet 13:440–444PubMedCrossRef Hunt KA, McGovern DP, Kumar PJ et al (2005) A common CTLA4 haplotype associated with coeliac disease. Eur J Hum Genet 13:440–444PubMedCrossRef
62.
Zurück zum Zitat Amundsen SS, Naluai AT, Ascher H et al (2004) Genetic analysis of the CD28/CTLA4/ICOS (CELIAC3) region in coeliac disease. Tissue Antigens 64:593–599PubMedCrossRef Amundsen SS, Naluai AT, Ascher H et al (2004) Genetic analysis of the CD28/CTLA4/ICOS (CELIAC3) region in coeliac disease. Tissue Antigens 64:593–599PubMedCrossRef
63.
Zurück zum Zitat Seidl C, Donner H, Fischer B et al (1998) CTLA4 codon 17 dimorphism in patients with rheumatoid arthritis. Tissue Antigens 51:62–66PubMedCrossRef Seidl C, Donner H, Fischer B et al (1998) CTLA4 codon 17 dimorphism in patients with rheumatoid arthritis. Tissue Antigens 51:62–66PubMedCrossRef
64.
Zurück zum Zitat Jung MH, Yu J, Shin CH, Suh BK, Yang SW, Lee BC (2009) Association of cytotoxic T lymphocyte antigen-4 gene polymorphisms and HLA class II alleles with the development of type 1 diabetes in Korean children and adolescents. J Korean Med Sci 24:1004–1009PubMedCrossRef Jung MH, Yu J, Shin CH, Suh BK, Yang SW, Lee BC (2009) Association of cytotoxic T lymphocyte antigen-4 gene polymorphisms and HLA class II alleles with the development of type 1 diabetes in Korean children and adolescents. J Korean Med Sci 24:1004–1009PubMedCrossRef
65.
Zurück zum Zitat Harper K, Balzano C, Rouvier E, Mattei MG, Luciani MF, Golstein P (1991) CTLA-4 and CD28 activated lymphocyte molecules are closely related in both mouse and human as to sequence, message expression, gene structure, and chromosomal location. J Immunol 147:1037–1044PubMed Harper K, Balzano C, Rouvier E, Mattei MG, Luciani MF, Golstein P (1991) CTLA-4 and CD28 activated lymphocyte molecules are closely related in both mouse and human as to sequence, message expression, gene structure, and chromosomal location. J Immunol 147:1037–1044PubMed
66.
Zurück zum Zitat Karandikar NJ, Vanderlugt CL, Walunas TL, Miller SD, Bluestone JA (1996) CTLA-4: a negative regulator of autoimmune disease. J Exp Med 184:783–788PubMedCrossRef Karandikar NJ, Vanderlugt CL, Walunas TL, Miller SD, Bluestone JA (1996) CTLA-4: a negative regulator of autoimmune disease. J Exp Med 184:783–788PubMedCrossRef
67.
Zurück zum Zitat Krummel MF, Allison JP (1996) CTLA-4 engagement inhibits IL-2 accumulation and cell cycle progression upon activation of resting T cells. J Exp Med 183:2533–2540PubMedCrossRef Krummel MF, Allison JP (1996) CTLA-4 engagement inhibits IL-2 accumulation and cell cycle progression upon activation of resting T cells. J Exp Med 183:2533–2540PubMedCrossRef
68.
Zurück zum Zitat Alegre ML, Shiels H, Thompson CB, Gajewski TF (1998) Expression and function of CTLA-4 in Th1 and Th2 cells. J Immunol 161:3347–3356PubMed Alegre ML, Shiels H, Thompson CB, Gajewski TF (1998) Expression and function of CTLA-4 in Th1 and Th2 cells. J Immunol 161:3347–3356PubMed
69.
Zurück zum Zitat Kouki T, Sawai Y, Gardine CA, Fisfalen ME, Alegre ML, DeGroot LJ (2000) CTLA-4 gene polymorphism at position 49 in exon 1 reduces the inhibitory function of CTLA-4 and contributes to the pathogenesis of Graves’ disease. J Immunol 165:6606–6611PubMed Kouki T, Sawai Y, Gardine CA, Fisfalen ME, Alegre ML, DeGroot LJ (2000) CTLA-4 gene polymorphism at position 49 in exon 1 reduces the inhibitory function of CTLA-4 and contributes to the pathogenesis of Graves’ disease. J Immunol 165:6606–6611PubMed
70.
Zurück zum Zitat Maurer M, Loserth S, Kolb-Maurer A et al (2002) A polymorphism in the human cytotoxic T-lymphocyte antigen 4 ( CTLA4) gene (exon 1 +49) alters T-cell activation. Immunogenetics 54:1–8PubMedCrossRef Maurer M, Loserth S, Kolb-Maurer A et al (2002) A polymorphism in the human cytotoxic T-lymphocyte antigen 4 ( CTLA4) gene (exon 1 +49) alters T-cell activation. Immunogenetics 54:1–8PubMedCrossRef
Metadaten
Titel
Interaction between CTLA4 gene and IBD5 locus in Hungarian Crohn’s disease patients
verfasst von
Veronika Csöngei
Luca Járomi
Enikő Sáfrány
Csilla Sipeky
Lili Magyari
Noémi Polgár
Judit Bene
Patrícia Sarlós
Lilla Lakner
Eszter Baricza
Melinda Szabó
Gábor Rappai
Béla Melegh
Publikationsdatum
01.09.2011
Verlag
Springer-Verlag
Erschienen in
International Journal of Colorectal Disease / Ausgabe 9/2011
Print ISSN: 0179-1958
Elektronische ISSN: 1432-1262
DOI
https://doi.org/10.1007/s00384-011-1202-z

Weitere Artikel der Ausgabe 9/2011

International Journal of Colorectal Disease 9/2011 Zur Ausgabe

Wie erfolgreich ist eine Re-Ablation nach Rezidiv?

23.04.2024 Ablationstherapie Nachrichten

Nach der Katheterablation von Vorhofflimmern kommt es bei etwa einem Drittel der Patienten zu Rezidiven, meist binnen eines Jahres. Wie sich spätere Rückfälle auf die Erfolgschancen einer erneuten Ablation auswirken, haben Schweizer Kardiologen erforscht.

Hinter dieser Appendizitis steckte ein Erreger

23.04.2024 Appendizitis Nachrichten

Schmerzen im Unterbauch, aber sonst nicht viel, was auf eine Appendizitis hindeutete: Ein junger Mann hatte Glück, dass trotzdem eine Laparoskopie mit Appendektomie durchgeführt und der Wurmfortsatz histologisch untersucht wurde.

Mehr Schaden als Nutzen durch präoperatives Aussetzen von GLP-1-Agonisten?

23.04.2024 Operationsvorbereitung Nachrichten

Derzeit wird empfohlen, eine Therapie mit GLP-1-Rezeptoragonisten präoperativ zu unterbrechen. Eine neue Studie nährt jedoch Zweifel an der Notwendigkeit der Maßnahme.

Ureterstriktur: Innovative OP-Technik bewährt sich

19.04.2024 EAU 2024 Kongressbericht

Die Ureterstriktur ist eine relativ seltene Komplikation, trotzdem bedarf sie einer differenzierten Versorgung. In komplexen Fällen wird dies durch die roboterassistierte OP-Technik gewährleistet. Erste Resultate ermutigen.

Update Chirurgie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

S3-Leitlinie „Diagnostik und Therapie des Karpaltunnelsyndroms“

Karpaltunnelsyndrom BDC Leitlinien Webinare
CME: 2 Punkte

Das Karpaltunnelsyndrom ist die häufigste Kompressionsneuropathie peripherer Nerven. Obwohl die Anamnese mit dem nächtlichen Einschlafen der Hand (Brachialgia parästhetica nocturna) sehr typisch ist, ist eine klinisch-neurologische Untersuchung und Elektroneurografie in manchen Fällen auch eine Neurosonografie erforderlich. Im Anfangsstadium sind konservative Maßnahmen (Handgelenksschiene, Ergotherapie) empfehlenswert. Bei nicht Ansprechen der konservativen Therapie oder Auftreten von neurologischen Ausfällen ist eine Dekompression des N. medianus am Karpaltunnel indiziert.

Prof. Dr. med. Gregor Antoniadis
Berufsverband der Deutschen Chirurgie e.V.

S2e-Leitlinie „Distale Radiusfraktur“

Radiusfraktur BDC Leitlinien Webinare
CME: 2 Punkte

Das Webinar beschäftigt sich mit Fragen und Antworten zu Diagnostik und Klassifikation sowie Möglichkeiten des Ausschlusses von Zusatzverletzungen. Die Referenten erläutern, welche Frakturen konservativ behandelt werden können und wie. Das Webinar beantwortet die Frage nach aktuellen operativen Therapiekonzepten: Welcher Zugang, welches Osteosynthesematerial? Auf was muss bei der Nachbehandlung der distalen Radiusfraktur geachtet werden?

PD Dr. med. Oliver Pieske
Dr. med. Benjamin Meyknecht
Berufsverband der Deutschen Chirurgie e.V.

S1-Leitlinie „Empfehlungen zur Therapie der akuten Appendizitis bei Erwachsenen“

Appendizitis BDC Leitlinien Webinare
CME: 2 Punkte

Inhalte des Webinars zur S1-Leitlinie „Empfehlungen zur Therapie der akuten Appendizitis bei Erwachsenen“ sind die Darstellung des Projektes und des Erstellungswegs zur S1-Leitlinie, die Erläuterung der klinischen Relevanz der Klassifikation EAES 2015, die wissenschaftliche Begründung der wichtigsten Empfehlungen und die Darstellung stadiengerechter Therapieoptionen.

Dr. med. Mihailo Andric
Berufsverband der Deutschen Chirurgie e.V.