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Abstract
Elevated constitutive expression of major histocompatability (MHC) class II antigens occurs in the enterocytes of patients with IBD. It has been suggested that this aberrant expression of class II molecules may play a role in the pathogenesis of IBD. We examined two possible reasons for such a finding. I) Heightened sensitivity of IBD enterocytes to endogenous γ interferon (γIFN) and 2) enhanced endogenous secretion of γ interferon by intestinal cells in close proximity to the enterocytes (lamina propria lymphocytes). Constitutive and γ interferon stimulated HLA-DR and DP density on intestinal epithelial cells (IEC) and peripheral blood monocytes (PBM) from UC patients (IEC n = 13; PBM n = 20), CD patients (IEC n = 14; PBM n = 18) and non-IBD controls (IEC n = 12; PBM n = 20) were measured via flow cytometry (mean channel fluorescence). γIFN production by PHA stimulated and unstimulated lamina propria lymphocyte (LPL) cultures of UC patients (n = 11) CD patients (n = 8) and non-IBD controls (n = 11) was measured using a vesicular stomatitis virus/WISH cell bioassay. We found significantly greater γIFN secretion by IBD-derived PHA stimulated LPL than from non-IBD stimulated controls (CD = 39.4 ± 12.4u; UC 41.5 ± 6.8u; NL = 22.4 ± 8.3u, p < 0.05) while γIFN induced HLA-DR and DP upregulation was no greater in IBD-derived IEC and PBM than in non-IBD controls. We conclude that the elevated constitutive MHC class II expression found in IBD enterocytes is not due to hypersensitivity of these cells to γIFN but is instead due, in part, to greater γIFN secretion by adjacent lamina propria lymphocytes.