scholarly journals ERAAP Synergizes with MHC Class I Molecules to Make the Final Cut in the Antigenic Peptide Precursors in the Endoplasmic Reticulum

Immunity ◽  
2006 ◽  
Vol 25 (5) ◽  
pp. 795-806 ◽  
Author(s):  
Takayuki Kanaseki ◽  
Nicolas Blanchard ◽  
Gianna Elena Hammer ◽  
Federico Gonzalez ◽  
Nilabh Shastri
Keyword(s):  
Endoplasmic Reticulum ◽  
Mhc Class I ◽  
Class I ◽  
Antigenic Peptide ◽  
Peptide Precursors ◽  
Mhc Class I Molecules

scholarly journals Release from Endoplasmic Reticulum Matrix Proteins Controls Cell Surface Transport of MHC Class I Molecules

Traffic ◽  
2015 ◽  
Vol 16 (6) ◽  
pp. 591-603 ◽  
Author(s):  
Susanne Fritzsche ◽  
Esam T. Abualrous ◽  
Britta Borchert ◽  
Frank Momburg ◽  
Sebastian Springer
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Surface ◽  
Mhc Class I ◽  
Matrix Proteins ◽  
Class I ◽  
Surface Transport ◽  
Mhc Class I Molecules

scholarly journals Modulation of Transporter Associated with Antigen Processing (TAP)-Mediated Peptide Import into the Endoplasmic Reticulum by Flavivirus Infection

2001 ◽  
Vol 75 (12) ◽  
pp. 5663-5671 ◽  
Author(s):  
Frank Momburg ◽  
Arno Müllbacher ◽  
Mario Lobigs
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Surface ◽  
Mhc Class I ◽  
Antigen Processing ◽  
Surface Expression ◽  
Class I ◽  
Peptide Transport ◽  
Cell Surface Expression ◽  
Flavivirus Infection ◽  
Mhc Class I Molecules

ABSTRACT In contrast to many other viruses that escape the cellular immune response by downregulating major histocompatibility complex (MHC) class I molecules, flavivirus infection can upregulate their cell surface expression. Previously we have presented evidence that during flavivirus infection, peptide supply to the endoplasmic reticulum is increased (A. Müllbacher and M. Lobigs, Immunity 3:207–214, 1995). Here we show that during the early phase of infection with different flaviviruses, the transport activity of the peptide transporter associated with antigen processing (TAP) is augmented by up to 50%. TAP expression is unaltered during infection, and viral but not host macromolecular synthesis is required for enhanced peptide transport. This study is the first demonstration of transient enhancement of TAP-dependent peptide import into the lumen of the endoplasmic reticulum as a consequence of a viral infection. We suggest that the increased supply of peptides for assembly with MHC class I molecules in flavivirus-infected cells accounts for the upregulation of MHC class I cell surface expression with the biological consequence of viral evasion of natural killer cell recognition.

scholarly journals Identification of human cancers deficient in antigen processing.

1993 ◽  
Vol 177 (2) ◽  
pp. 265-272 ◽  
Author(s):  
N P Restifo ◽  
F Esquivel ◽  
Y Kawakami ◽  
J W Yewdell ◽  
J J Mulé ◽  
...  
Keyword(s):  
T Cells ◽  
Endoplasmic Reticulum ◽  
Mhc Class I ◽  
Cell Lines ◽  
Antigen Processing ◽  
Human Tumor ◽  
Class I ◽  
Cell Lung Carcinoma ◽  
Mhc Molecules ◽  
Mhc Class I Molecules

Intracellular antigens must be processed before presentation to CD8+ T cells by major histocompatibility complex (MHC) class I molecules. Using a recombinant vaccinia virus (Vac) to transiently express the Kd molecule, we studied the antigen processing efficiency of 26 different human tumor lines. Three cell lines, all human small cell lung carcinoma, consistently failed to process endogenously synthesized proteins for presentation to Kd-restricted, Vac-specific T cells. Pulse-chase experiments showed that MHC class I molecules were not transported by these cell lines from the endoplasmic reticulum to the cell surface. This finding suggested that peptides were not available for binding to nascent MHC molecules in the endoplasmic reticulum. Northern blot analysis of these cells revealed low to nondetectable levels of mRNAs for MHC-encoded proteasome components LMP-7 and LMP-2, as well as the putative peptide transporters TAP-1 and TAP-2. Treatment of cells with interferon gamma enhanced expression of these mRNAs and reversed the observed functional and biochemical deficits. Our findings suggest that downregulation of antigen processing may be one of the strategies used by tumors to escape immune surveillance. Potential therapeutic applications of these findings include enhancing antigen processing at the level of the transcription of MHC-encoded proteasome and transporter genes.

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