The coronavirus SARS-CoV-2 contributes to morbidity and mortality mainly as a result of immune-pathology in the lungs. Recent data has shown multi-system involvement with widespread viral tropism. Here we present a detailed intestinal protein characterisation of SARS-Cov-2 entry molecules ACE2 and TMPRSS2 in patients with Inflammatory Bowel Disease ([IBD]; Ulcerative Colitis [UC] and Crohn’s disease [CD]) with age- and sex-match non-IBD controls; and in those with fatal COVID19 infection. Our study showed that IBD gut inflammation did not influence ACE2 and TRPMSS2 expression. Of interest, colonic protein expression of ACE2 and TRPMSS2 are cytoplasmic distinct to the membranous pattern in the ileum. We observed a significant increase in immune cells within the lamina propria in UC and CD that expressed ACE2 and TRMPSS2 when compared to non-IBD controls. These were identified as plasma cells with multiple myeloma oncogene 1/interferon regulatory factor 4 (MUM1/IRF4) expression. In six fatal COVID19 cases, there was no gut inflammation despite evidence of viral tropism within the enterocytes. Our data provides evidence for tissue expression of entry molecules ACE2 and TMPRSS2 including a close apposition to plasma cells – both pointing towards a role of the gut in the immune response to SARS-CoV-2 infection.