scholarly journals Antigen Presentation in the Gut

1990 ◽  
Vol 4 (7) ◽  
pp. 267-270 ◽  
Author(s):  
W Doe ◽  
P Pavli
Keyword(s):  
Dendritic Cells ◽  
Epithelial Cells ◽  
Immune Responses ◽  
Antigen Presentation ◽  
Class Ii ◽  
T Helper ◽  
Colonic Epithelial Cells ◽  
Mhc Molecules ◽  
Class Ii Mhc ◽  
Antigen Presenting

The induction of T cell responses requires recognition of antigens in association with class II major histocompatibility complex (MHC) proteins and specialized antigen-presenting cells. Candidate antigen-presenting cells in the gut include dendritic cells, macrophages, B lymphocytes, mucosal epithelial cells and endothelial cells. Dendritic cells isolated from normal human colon are potent inducers of primary immune responses and express high levels of class lI MHC proteins. Lamina propria macrophages display class II MHC proteins, can present antigens to sensitized T cells, may process antigen and release interleukin-l, but suppress antigen presentation by intestinal dendritic cells in a dose-dependent manner. Class II MHC molecules are normally expressed on small intestinal epithelial cells but not on normal colonic epithelial cells. Suppressor T cells and unresponsive T helper cells in the mucosa appear to mediate systemic T cell tolerance of dietary antigens. In the inflamed colon there is infiltration of the lamina propria by large numbers of monocytes which secrete interleukin-1, and the release of interferon-gamma appears to induce class II protein expression on colonic epithelial cells. Colonic epithelial cells from inflamed bowel may preferentially stimulate T helper cells so that local induction of class II MHC molecules on epithelial cells may amplify and localize secondary immune responses at the site of inflamed mucosa. Taken together, the aberrant expression of class II MHC molecules, breaches in epithelial cell integrity (resulting m exposure to luminal antigens including endotoxin and the increased numbers of monocytes found 10 inflamed mucosa suggest that the resulting distortions in antigen presentation contribute to the localization and persistence of the inflammatory lesion in inflammatory bowel disease.

scholarly journals Presence and regulation of messenger ribonucleic acids encoding components of the class II major histocompatibility complex-associated antigen processing pathway in the bovine corpus luteum

Reproduction ◽  
2006 ◽  
Vol 131 (4) ◽  
pp. 689-698 ◽  
Author(s):  
Matthew J Cannon ◽  
John S Davis ◽  
Joy L Pate
Keyword(s):  
Corpus Luteum ◽  
Estrous Cycle ◽  
Antigen Processing ◽  
Class Ii ◽  
Luteal Cells ◽  
Mhc Molecules ◽  
Histocompatibility Complex ◽  
Class Ii Mhc ◽  
Luteal Tissue ◽  
Antigen Presenting

Luteal cells express class II major histocompatibility complex (MHC) molecules and can stimulate T lymphocyte proliferationin vitro. However, it is unknown whether luteal cells express the intracellular components necessary to process the peptides presented by class II MHC molecules. The objective of the present study was to examine the expression and regulation of three major class II-associated antigen processing components – class II MHC-associated invariant chain (Ii), DMα and DMβ – in luteal tissue. Corpora lutea were collected early in the estrous cycle, during midcycle and late in the estrous cycle, and at various times following administration of a luteolytic dose of prostaglandin F2α(PGF2α) to the cow. Northern analysis revealed the presence of mRNA encoding each of the class II MHC-associated antigen processing proteins in luteal tissue. Ii mRNA concentrations did not change during the estrous cycle, whereas DMα and DMβ mRNA concentrations were highest in midcycle luteal tissue compared with either early or late luteal tissue. Tumor necrosis factor-α (TNF-α) reduced DMα mRNA concentrations in cultured luteal cells in the presence of LH or PGF2α. DMα and DMβ mRNA were also present in highly enriched cultures of luteal endothelial (CLENDO) cells, and DMα mRNA concentrations were greater in CLENDO cultures compared with mixed luteal cell cultures. Expression of invariant chain, DMα and DMβ genes indicates that cells within the corpus luteum express the minimal requirements to act as functional antigen-presenting cells, and the observation that CLENDO cells are a source of DMα and DMβ mRNA indicates that non-immune cells within the corpus luteum may function as antigen-presenting cells.

Competition for antigen presentation in living cells involves exchange of peptides bound by class II MHC molecules

Nature ◽  
1989 ◽  
Vol 342 (6251) ◽  
pp. 800-803 ◽  
Author(s):  
Luciano Adorini ◽  
Ettore Appella ◽  
Gino Doria ◽  
Francis Cardinaux ◽  
Zoltan A. Nagy
Keyword(s):  
Antigen Presentation ◽  
Class Ii ◽  
Living Cells ◽  
Mhc Molecules ◽  
Class Ii Mhc

scholarly journals Polarized Expression of CD74 by Gastric Epithelial Cells

2005 ◽  
Vol 53 (12) ◽  
pp. 1481-1489 ◽  
Author(s):  
Carlos A. Barrera ◽  
Ellen J. Beswick ◽  
Johanna C. Sierra ◽  
David Bland ◽  
Rosario Espejo ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mhc Class Ii ◽  
Cell Biology ◽  
Constitutive Expression ◽  
Class Ii ◽  
Protein Isoforms ◽  
Apical Surface ◽  
Gastric Epithelial Cells ◽  
Mhc Molecules ◽  
Class Ii Mhc

CD74 is known as the major histocompatibility complex (MHC) class II-associated invariant chain (Ii) that regulates the cell biology and functions of MHC class II molecules. Class II MHC and Ii expression was believed to be restricted to classical antigen-presenting cells (APC); however, during inflammation, other cell types, including mucosal epithelial cells, have also been reported to express class II MHC molecules. Given the importance of Ii in the biology of class II MHC, we sought to examine the expression of Ii by gastric epithelial cells (GEC) to determine whether class II MHC molecules in these nonconventional APC cells were under the control of Ii and to further support the role that these cells may play in local immune and inflammatory responses during Helicobacter pylori infection. Thus we examined the expression of Ii on GEC from human biopsy samples and then confirmed this observation using independent methods on several GEC lines. The mRNA for Ii was detected by RT-PCR, and the various protein isoforms were also detected. Interestingly, these cells have a high level expression of surface Ii, which is polarized to the apical surface. These studies are the first to demonstrate the constitutive expression of Ii by human GEC.

Class II MHC/Peptide Complexes on T Cell Antigen-Presenting Cells: Agonistic Antigen Recognition Inhibits Subsequent Antigen Presentation

1998 ◽  
Vol 186 (2) ◽  
pp. 111-120 ◽  
Author(s):  
Mark D. Mannie ◽  
John P. Nardella ◽  
Gregory A. White ◽  
Paula Y. Arnold ◽  
Daniel K. Davidian
Keyword(s):  
T Cell ◽  
Antigen Presentation ◽  
Antigen Presenting Cells ◽  
Class Ii ◽  
Antigen Recognition ◽  
Cell Antigen ◽  
Class Ii Mhc ◽  
Peptide Complexes ◽  
Antigen Presenting

scholarly journals The Effect of Class II Major Histocompatibility Complex Expression on Adherence of Helicobacter pylori and Induction of Apoptosis in Gastric Epithelial Cells: A Mechanism for T Helper Cell Type 1–mediated Damage

1998 ◽  
Vol 187 (10) ◽  
pp. 1659-1669 ◽  
Author(s):  
Xuejun Fan ◽  
Sheila E. Crowe ◽  
Simon Behar ◽  
Harshani Gunasena ◽  
Gang Ye ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Class Ii ◽  
Gastric Epithelial Cells ◽  
Mhc Molecules ◽  
Histocompatibility Complex ◽  
Class Ii Mhc ◽  
Ifn Γ ◽  
Induction Of Apoptosis ◽  
H Pylori

Helicobacter pylori infection is associated with gastric epithelial damage, including apoptosis, ulceration, and cancer. Although bacterial factors and the host response are believed to contribute to gastric disease, no receptor has been identified that explains how the bacteria attach and signal the host cell to undergo apoptosis. Using H. pylori as “bait” to capture receptor proteins in solubilized membranes of gastric epithelial cells, class II major histocompatibility complex (MHC) molecules were identified as a possible receptor. Signaling through class II MHC molecules leading to the induction of apoptosis was confirmed using cross-linking IgM antibodies to surface class II MHC molecules. Moreover, binding of H. pylori and the induction of apoptosis were inhibited by antibodies recognizing class II MHC. Since type 1 T helper cells are present during infection and produce interferon (IFN)-γ, which increases class II MHC expression, gastric epithelial cell lines were exposed to H. pylori in the presence or absence of IFN-γ. IFN-γ increased the attachment of the bacteria as well as the induction of apoptosis in gastric epithelial cells. In contrast to MHC II–negative cell lines, H. pylori induced apoptosis in cells expressing class II MHC molecules constitutively or after gene transfection. These data describe a novel receptor for H. pylori and provide a mechanism by which bacteria and the host response interact in the pathogenesis of gastric epithelial cell damage.

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