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    Major histocompatibility complex class II inhibits fas antigen-mediated gastric mucosal cell apoptosis through actin-dependent inhibition of receptor aggregation

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    Authors
    Stoicov, Calin
    Cai, Xun
    Li, Hanchen
    Klucevsek, Kristine
    Carlson, Jane E.
    Saffari, Reza
    Houghton, JeanMarie
    Student Authors
    Calin Stoicov
    UMass Chan Affiliations
    Department of Medicine, Division of Gastroenterology
    Document Type
    Journal Article
    Publication Date
    2005-09-24
    Keywords
    Actins; Animals; Antigens, CD95; Apoptosis; Cells, Cultured; Cytochalasin D; Gastric Mucosa; Helicobacter Infections; Helicobacter felis; Helicobacter pylori; Histocompatibility Antigens Class II; Interferon Type II; Male; Mice; Mice, Inbred C57BL; Rats; *Receptor Aggregation; Signal Transduction
    Gastroenterology
    Life Sciences
    Medicine and Health Sciences
    
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    Link to Full Text
    http://dx.doi.org/10.1128/IAI.73.10.6311-6321.2005
    Abstract
    Escape from normal apoptotic controls is thought to be essential for the development of cancer. During Helicobacter pylori infection, the leading cause of gastric cancer, activation of the Fas antigen (Fas Ag) apoptotic pathway is responsible for early atrophy and tissue loss. As disease progresses, metaplastic and dysplastic glands arise which express Fas Ag but are resistant to apoptosis and are believed to be the precursor cells for adenocarcinoma. In this report, we show that one mechanism of acquired Fas resistance is inhibition of receptor aggregation via a major histocompatibility complex class II (MHCII)-mediated, actin-dependent mechanism. For these studies we used the well-described C57BL/6 mouse model of Helicobacter pylori and Helicobacter felis infection. Under normal conditions, Fas Ag is expressed at low levels, and MHCII expression on gastric mucosal cells is negligible. With infection and inflammation, both receptors are upregulated, and 6.1% of gastric mucosal cells express MHCII in combination with Fas Ag. Using the rat gastric mucosal cell line RGM-1 transfected with murine Fas Ag and MHCIIalphabeta chains, we demonstrate that MHCII prevents Fas receptor aggregation and inhibits Fas-mediated signaling through its effects on the actin cytoskeleton. Depolymerization of actin with cytochalasin D allows receptors to aggregate and restores Fas sensitivity. These findings offer one mechanism by which gastric mucosal cells acquire Fas resistance.
    Source
    Infect Immun. 2005 Oct;73(10):6311-21. Link to article on publisher's site
    DOI
    10.1128/IAI.73.10.6311-6321.2005
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/32645
    PubMed ID
    16177302
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1128/IAI.73.10.6311-6321.2005
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    Morningside Graduate School of Biomedical Sciences Scholarly Publications

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