Jostins, LukeRipke, StephanWeersma, Rinse KDuerr, Richard HMcGovern, Dermot PHui, Ken YLee, James CSchumm, L PhilipSharma, YashodaAnderson, Carl AEssers, Jonah BryanMitrovic, MitjaNing, KaidaCleynen, IsabelleTheatre, EmilieSpain, Sarah LRaychaudhuri, SoumyaGoyette, PhilippeWei, ZhiAbraham, ClaraAchkar, Jean-PaulAhmad, TariqAmininejad, LeilaAnanthakrishnan, AshwinAndersen, VibekeAndrews, Jane MBaidoo, LeonardBalschun, TobiasBampton, Peter ABitton, AlainBoucher, GabrielleBrand, StephanBüning, CarstenCohain, AriellaCichon, SvenD’Amato, MauroDe Jong, DirkDevaney, Kathy LDubinsky, MarlaEdwards, CathrynEllinghaus, DavidFerguson, Lynnette RFranchimont, DenisFransen, KarinGearry, RichardGeorges, MichelGieger, ChristianGlas, JürgenHaritunians, TalinHart, AilsaHawkey, ChrisHedl, MatijaHu, XinliKarlsen, Tom HKupcinskas, LimasKugathasan, SubraLatiano, AnnaLaukens, DebbyLawrance, Ian CLees, Charlie WLouis, EdouardMahy, GillianMansfield, JohnMorgan, Angharad RMowat, CraigNewman, WilliamPalmieri, OrazioPonsioen, Cyriel YPotocnik, UrosPrescott, Natalie JRegueiro, MiguelRotter, Jerome IRussell, Richard KSanderson, Jeremy DSans, MiquelSatsangi, JackSchreiber, StefanSimms, Lisa ASventoraityte, JurgitaTargan, Stephan RTaylor, Kent DTremelling, MarkVerspaget, Hein WDe Vos, MartineWijmenga, CiscaWilson, David CWinkelmann, JulianeXavier, RamnikZeissig, SebastianZhang, BinZhang, Clarence KZhao, HongyuSilverberg, Mark SAnnese, VitoHakonarson, HakonBrant, Steven RRadford-Smith, GrahamMathew, Christopher GRioux, John DSchadt, Eric EDaly, MarkFranke, AndreParkes, MilesVermeire, SeverineBarrett, Jeffrey CCho, Judy H2013-10-172012Jostins, Luke, Stephan Ripke, Rinse K Weersma, Richard H Duerr, Dermot P McGovern, Ken Y Hui, James C Lee, et al. 2012. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature 491(7422): 119-124.0028-0836http://nrs.harvard.edu/urn-3:HUL.InstRepos:11181023Crohn’s disease (CD) and ulcerative colitis (UC), the two common forms of inflammatory bowel disease (IBD), affect over 2.5 million people of European ancestry with rising prevalence in other populations1. Genome-wide association studies (GWAS) and subsequent meta-analyses of CD and UC2,3 as separate phenotypes implicated previously unsuspected mechanisms, such as autophagy4, in pathogenesis and showed that some IBD loci are shared with other inflammatory diseases5. Here we expand knowledge of relevant pathways by undertaking a meta-analysis of CD and UC genome-wide association scans, with validation of significant findings in more than 75,000 cases and controls. We identify 71 new associations, for a total of 163 IBD loci that meet genome-wide significance thresholds. Most loci contribute to both phenotypes, and both directional and balancing selection effects are evident. Many IBD loci are also implicated in other immune-mediated disorders, most notably with ankylosing spondylitis and psoriasis. We also observe striking overlap between susceptibility loci for IBD and mycobacterial infection. Gene co-expression network analysis emphasizes this relationship, with pathways shared between host responses to mycobacteria and those predisposing to IBD.en-USJournal Article2013-10-1710.1038/nature11582