Abstract
Inflammatory Bowel Disease (IBD), which includes Crohn’s Disease (CD) and Ulcerative Colitis (UC), has a heterogeneous pathogenesis underlined by genetic predisposition, intestinal barrier dysfunction, impaired immune response, and microbiota imbalance.
Highlights
Inflammatory Bowel Disease (IBD), which includes Crohn’s Disease (CD) and Ulcerative Colitis (UC), has a heterogeneous pathogenesis underlined by genetic predisposition, intestinal barrier dysfunction, impaired immune response, and microbiota imbalance [1,2,3]
Using publicly available transcriptomes obtained from large number of UC patients from European and the US cohorts [8,9,10,11,12,13,14,15,16], we identified systemic immune cell landscape, pathways, and transcriptional signatures specific for UC as well as those determining outcome of biologic therapy [17]
UC tissue obtained from patients prior to biologic therapy with anti-TNFα and anti-α4β7, which were later identified clinically as non-responders, had considerably more neutrophils and T CD4 activated cells when compared to responders
Summary
Inflammatory Bowel Disease (IBD), which includes Crohn’s Disease (CD) and Ulcerative Colitis (UC), has a heterogeneous pathogenesis underlined by genetic predisposition, intestinal barrier dysfunction, impaired immune response, and microbiota imbalance [1,2,3]. This proceeds to aberrant immune cells presence and function in the affected tissue, activation of signaling pathways, and expression of regulators that subsequently drive inflammation [2,4,5,6,7]. Using publicly available transcriptomes obtained from large number of UC patients from European and the US cohorts [8,9,10,11,12,13,14,15,16], we identified systemic immune cell landscape, pathways, and transcriptional signatures specific for UC as well as those determining outcome of biologic therapy [17].
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