Synergistic effect between IL-10 and bcl-2 genotypes in determining susceptibility to systemic lupus erythematosus

Arthritis and Rheumatism
R MehrianC O Jacob

Abstract

To determine whether genes participating in programmed cell death, including bcl-2, IL-10, Fas-L, and CTLA-4, may contribute to the genetic predisposition to systemic lupus erythematosus (SLE). First, intragenic markers for the bcl-2, IL-10, Fas-L, and CTLA-4 genes were characterized and their extent of polymorphism in normal populations was determined. The allelic distribution of these gene markers in a large Mexican American SLE cohort of 158 patients and 223 ethnically matched controls was determined using fluorescent-labeled primers and semiautomated genotyping. The bcl-2, Fas-L, and IL-10 loci showed significantly different allelic distribution in SLE patients compared with controls, indicating an association between these genes and SLE. No association was found between SLE and the CTLA-4 gene. Further analysis revealed a synergistic effect between susceptibility alleles of the bcl-2 and IL-10 genes in determining disease susceptibility. Alone, the presence of each of these alleles was associated with a moderate increase in SLE risk, while the occurrence of these alleles together increased the odds of developing SLE by more than 40-fold. The results suggest that individuals carrying specific genotypes of both bcl-2 and IL-...Continue Reading

References

Aug 1, 1992·Immunology Today·S J Korsmeyer
Jul 25, 1991·Nucleic Acids Research·M H PolymeropoulosC R Merril
Jul 25, 1991·Nucleic Acids Research·M H PolymeropoulosC R Merril
Oct 1, 1991·Proceedings of the National Academy of Sciences of the United States of America·A StrasserA W Harris
Nov 1, 1982·Arthritis and Rheumatism·E M TanR J Winchester
Oct 1, 1994·Arthritis and Rheumatism·J D MountzT Zhou
Mar 10, 1995·Science·S Nagata, P Golstein
Oct 1, 1994·Journal of Autoimmunity·P A Gatenby, M Irvine
Jan 31, 1995·Proceedings of the National Academy of Sciences of the United States of America·J G GribbenG S Gray
Jul 1, 1994·The Journal of Clinical Investigation·K TagaG Tosato
Jan 1, 1994·The Journal of Clinical Investigation·Y Levy, J C Brouet
Dec 1, 1993·International Immunology·K TagaG Tosato
Jan 1, 1993·Annual Review of Immunology·K W MooreT R Mosmann
Dec 1, 1995·Current Opinion in Immunology·T R Merriman, J A Todd
Dec 1, 1995·Current Opinion in Immunology
Feb 1, 1997·European Journal of Immunogenetics : Official Journal of the British Society for Histocompatibility and Immunogenetics·D M TurnerI V Hutchinson
Feb 15, 1997·The Journal of Clinical Investigation·B L Kotzin
Feb 15, 1997·The Journal of Clinical Investigation·B P TsaoJ I Rotter

❮ Previous
Next ❯

Citations

Mar 3, 2011·Cell Death & Disease·D TischnerA Villunger
Nov 10, 2010·Nature Reviews. Rheumatology·Yun Deng, Betty P Tsao
Aug 14, 1999·Immunology·B J RipleyD S Latchman
Mar 25, 2000·Annals of the Rheumatic Diseases·G S DeanD A Isenberg
Apr 20, 1999·The Journal of Clinical Investigation·B P TsaoJ I Rotter
Mar 1, 2000·Proceedings of the National Academy of Sciences of the United States of America·M S BynoeB Diamond
Jul 14, 2010·Journal of Biomedicine & Biotechnology·Patricia LópezAna Suárez
May 15, 2009·Genes and Immunity·D L ArmstrongC O Jacob
Oct 4, 2000·International Reviews of Immunology·B P Tsao
Oct 4, 2000·International Reviews of Immunology·F C Arnett
Dec 14, 2007·Autoimmunity·Bahram NamjouJohn B Harley
Jun 2, 2012·Journal of Biomedicine & Biotechnology·John J Connolly, Hakon Hakonarson
Apr 10, 2008·International Journal of Immunogenetics·S RosadoP Perez-Aciego
Jun 1, 2005·Rheumatic Diseases Clinics of North America·Andrea L SestakJohn B Harley
Oct 30, 2004·Current Opinion in Immunology·Swapan K NathJohn B Harley
Apr 21, 2004·Journal of the American Academy of Dermatology·Elliot WeissDaniel Nathan Sauder
Jul 21, 2004·Rheumatic Diseases Clinics of North America·Sophie KoutouzovZahir Amoura
Apr 18, 2000·Rheumatic Diseases Clinics of North America·K E Sullivan
Jan 12, 1999·Lupus·B P Tsao
Jan 20, 2010·Pharmaceuticals·Claudio Ponticelli, Gabriella Moroni
Sep 7, 2002·Genes and Immunity·J A KellyJ B Harley
Oct 6, 2006·Springer Seminars in Immunopathology·John B HarleyKenneth M Kaufman
Sep 10, 2004·Current Rheumatology Reports·Gabor G Illei, Peter E Lipsky
May 16, 2001·Current Rheumatology Reports·B P Tsao, J M Grossman

❮ Previous
Next ❯

Related Concepts

Related Feeds

BCL-2 Family Proteins

BLC-2 family proteins are a group that share the same homologous BH domain. They play many different roles including pro-survival signals, mitochondria-mediated apoptosis and removal or damaged cells. They are often regulated by phosphorylation, affecting their catalytic activity. Here is the latest research on BCL-2 family proteins.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis