Increased Th1/Th17 immune response is a hallmark of Crohn’s Disease (CD) Immunopathogenesis. CD90+ (myo)fibroblasts (CMF) are an abundant cells in colonic mucosa contributing to the mucosal tolerance via suppression of Th1 cell activity through PD-L1 signaling. CD-CMFs have decreased surface PD-L1, yet the mechanism responsible for this decrease is unknown. Increased expression of Matrix Metalloproteinases (MMPs), has been reported in CD. We hypothesize that increased MMP activity by CD-CMFs reduces cell surface level of PD-L1 contributing to the disruption of CMF-mediated suppression of Th1 type responses.