scholarly journals The Tetraspanin CD82 Is Specifically Recruited to Fungal and Bacterial Phagosomes prior to Acidification

2010 ◽  
Vol 79 (3) ◽  
pp. 1098-1106 ◽  
Author(s):  
Katerina Artavanis-Tsakonas ◽  
Pia V. Kasperkovitz ◽  
Eliseo Papa ◽  
Michael L. Cardenas ◽  
Nida S. Khan ◽  
...  
Keyword(s):  
Antigen Presentation ◽  
Cancer Metastasis ◽  
Physiological Role ◽  
Pathogenic Fungi ◽  
Class Ii ◽  
Endocytic Pathway ◽  
Mhc Molecules ◽  
Class Ii Mhc ◽  
Presentation Pathway ◽  
Partial Overlap

ABSTRACTCD82 is a member of the tetraspanin superfamily, whose physiological role is best described in the context of cancer metastasis. However, CD82 also associates with components of the class II major histocompatibility complex (MHC) antigen presentation pathway, including class II MHC molecules and the peptide-loading machinery, as well as CD63, another tetraspanin, suggesting a role for CD82 in antigen presentation. Here, we observe the dynamic rearrangement of CD82 after pathogen uptake by imaging CD82-mRFP1 expressed in primary living dendritic cells. CD82 showed rapid and specific recruitment toCryptococcus neoformans-containing phagosomes compared to polystyrene-containing phagosomes, similar to CD63. CD82 was also actively recruited to phagosomes containing other pathogenic fungi, includingCandida albicansandAspergillus fumigatus. Recruitment of CD82 to fungal phagosomes occurred independently of Toll-like receptor (TLR) signaling. Recruitment was not limited to fungi, as bacterial organisms, includingEscherichia coliandStaphylococcus aureus, also induced CD82 recruitment to the phagosome. CD82 intersected the endocytic pathway used by lipopolysaccharide (LPS), implicating CD82 in trafficking of small, pathogen-associated molecules. Despite its partial overlap with lysosomal compartments, CD82 recruitment toC. neoformans-containing phagosomes occurred independently of phagosome acidification. Kinetic analysis of fluorescence imaging revealed that CD82 and class II MHC simultaneously appear in the phagosome, indicating that the two proteins may be associated. Together, these data show that the CD82 tetraspanin is specifically recruited to pathogen-containing phagosomes prior to fusion with lysosomes.

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

Peptide and Peptide Mimetic Inhibitors of Antigen Presentation by HLA-DR Class II MHC Molecules. Design, Structure−Activity Relationships, and X-ray Crystal Structures

2000 ◽  
Vol 43 (11) ◽  
pp. 2135-2148 ◽  
Author(s):  
David R. Bolin ◽  
Amy L. Swain ◽  
Ramakanth Sarabu ◽  
Steven J. Berthel ◽  
Paul Gillespie ◽  
...  
Keyword(s):  
Antigen Presentation ◽  
Crystal Structures ◽  
Class Ii ◽  
X Ray ◽  
Structure Activity Relationships ◽  
Mhc Molecules ◽  
Structure Activity ◽  
Design Structure ◽  
Hla Dr ◽  
Class Ii Mhc

Class II MHC molecules can use the endogenous pathway of antigen presentation

Nature ◽  
1990 ◽  
Vol 343 (6253) ◽  
pp. 74-76 ◽  
Author(s):  
Jed G. Nuchtern ◽  
William E. Biddison ◽  
Richard D. Klausner
Keyword(s):  
Antigen Presentation ◽  
Class Ii ◽  
Mhc Molecules ◽  
Class Ii Mhc

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.

Electron microscopy analysis of degenerating pancreatic ß cells in transgenic mice expressing the MHC Class I antigen Dd

1990 ◽  
Vol 48 (3) ◽  
pp. 548-549
Author(s):  
T. A. Stewart ◽  
D. Liggitt ◽  
S. Pitts ◽  
L. Martin ◽  
M. Siegel ◽  
...  
Keyword(s):  
Type I Diabetes ◽  
Disease Process ◽  
Class Ii ◽  
Class I ◽  
Type I ◽  
Aberrant Expression ◽  
Mhc Molecules ◽  
Endogenous Insulin ◽  
Class Ii Mhc ◽  
Ifn Γ

Insulin-dependant (Type I) diabetes mellitus (IDDM) is a metabolic disorder resulting from the lack of endogenous insulin secretion. The disease is thought to result from the autoimmune mediated destruction of the insulin producing ß cells within the islets of Langerhans. The disease process is probably triggered by environmental agents, e.g. virus or chemical toxins on a background of genetic susceptibility associated with particular alleles within the major histocompatiblity complex (MHC). The relation between IDDM and the MHC locus has been reinforced by the demonstration of both class I and class II MHC proteins on the surface of ß cells from newly diagnosed patients as well as mounting evidence that IDDM has an autoimmune pathogenesis. In 1984, a series of observations were used to advance a hypothesis, in which it was suggested that aberrant expression of class II MHC molecules, perhaps induced by gamma-interferon (IFN γ) could present self antigens and initiate an autoimmune disease. We have tested some aspects of this model and demonstrated that expression of IFN γ by pancreatic ß cells can initiate an inflammatory destruction of both the islets and pancreas and does lead to IDDM.

MHC Sınıf I ve MHC Sınıf II Gen Düzenlenmesi

2020 ◽  
Vol 8 (3) ◽  
pp. 144-156
Author(s):  
Şule KARATAŞ ◽  
Fatma SAVRAN OĞUZ
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Gene Regulation ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Class I ◽  
Mhc Molecules ◽  
Class Ii Mhc ◽  
Regulation Mechanisms

Introduction: Peptides obtained by processing intracellular and extracellular antigens are presented to T cells to stimulate the immune response. This presentation is made by peptide receptors called major histocompatibility complex (MHC) molecules. The regulation mechanisms of MHC molecules, which have similar roles in the immune response, especially at the gene level, have significant differences according to their class. Objective: Class I and class II MHC molecules encoded by MHC genes on the short arm of the sixth chromosome are peptide receptors that stimulate T cell response. These peptides, which will enable the recognition of the antigen from which they originate, are loaded into MHC molecules and presented to T cells. Although the principles of loading and delivering peptides are similar for both molecules, the peptide sources and peptide loading mechanisms are different. In addition, class I molecules are expressed in all nucleated cells while class II molecules are expressed only in Antigen Presentation Cells (APC). These differences; It shows that MHC class I is not expressed by exactly the same transcriptional mechanisms as MHC class II. In our article, we aimed to compare the gene expressions of both classes and reveal their similarities and differences. Discussion and Conclusion: A better understanding of the transcriptional mechanisms of MHC molecules will reveal the role of these molecules in diseases more clearly. In our review, we discussed MHC gene regulation mechanisms with presence of existing informations, which is specific to the MHC class, for contribute to future research. Keywords: MHC class I, MHC class II, MHC gene regulation, promoter, SXY module, transcription

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