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Research Article Free access | 10.1172/JCI119739

Defective expression of gp180, a novel CD8 ligand on intestinal epithelial cells, in inflammatory bowel disease.

L S Toy, X Y Yio, A Lin, S Honig, and L Mayer

Division of Clinical Immunology, Mount Sinai Medical Center, New York 10029, USA.

Find articles by Toy, L. in: JCI | PubMed | Google Scholar

Division of Clinical Immunology, Mount Sinai Medical Center, New York 10029, USA.

Find articles by Yio, X. in: JCI | PubMed | Google Scholar

Division of Clinical Immunology, Mount Sinai Medical Center, New York 10029, USA.

Find articles by Lin, A. in: JCI | PubMed | Google Scholar

Division of Clinical Immunology, Mount Sinai Medical Center, New York 10029, USA.

Find articles by Honig, S. in: JCI | PubMed | Google Scholar

Division of Clinical Immunology, Mount Sinai Medical Center, New York 10029, USA.

Find articles by Mayer, L. in: JCI | PubMed | Google Scholar

Published October 15, 1997 - More info

Published in Volume 100, Issue 8 on October 15, 1997
J Clin Invest. 1997;100(8):2062–2071. https://doi.org/10.1172/JCI119739.
© 1997 The American Society for Clinical Investigation
Published October 15, 1997 - Version history
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Abstract

Previous studies support a role for intestinal epithelial cells (IEC) as antigen-presenting cells in mucosal immune responses. T cells activated by IEC are CD8+, suppressor in function, and dependent upon CD8-associated p56lck activation. A 180-kD glycoprotein (gp180) recognized by mAbs B9 and L12 has been identified and shown to be important in CD8+ T cell activation by IEC. Since IEC derived from patients with inflammatory bowel disease (IBD) are incapable of activating CD8+ T cells, we asked whether this correlated with gp180 expression. While frozen sections of normal bowel revealed bright gp180 staining on all IEC, both inflamed and uninflamed ulcerative colitis (UC) specimens showed patchy staining. In Crohn's disease (CD), staining was faint to absent. Flow cytometry confirmed immunohistochemical data. The staining patterns correlated with the ability of IEC to activate CD8-associated p56lck. Normal IEC induced phosphorylation of p56lck in CD8alpha but not CD4+ transfectants. In contrast, both UC and CD IEC activated CD4 and, to a much lesser extent, CD8-associated p56lck. Thus, gp180 expression by IBD IEC appears to be altered, and correlates with a functional alteration of lck activation. This defect may reflect a more proximal event in the pathogenesis of IBD.

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