Abstract
Current therapies to treat inflammatory bowel disease by dampening excessive inflammatory immune responses have had limited success ( Reinisch et al., 2011 ; Rutgeerts et al., 2005 ; Sandborn et al., 2012 ). To develop new therapeutic interventions, there is a need for better understanding of the mechanisms that are operative during mucosal healing (Pineton de Chambrun et al., 2010 ). To this end, a reversible model of colitis was developed in which colitis induced by adoptive transfer of naïve CD4+ CD45RBhi T cells in lymphopenic mice can be reversed through depletion of colitogenic CD4+ T cells ( Brasseit et al., 2016 ).