scholarly journals Ontogenic Appearance of MHC Class I (B-F) Antigens During Chicken Embryogenesis

1990 ◽  
Vol 1 (2) ◽  
pp. 127-135 ◽  
Author(s):  
D. Dunon ◽  
J. Salomonsen ◽  
K. Skjødt ◽  
J. Kaufman ◽  
B. A. Imhof
Keyword(s):  
Mhc Class I ◽  
Surface Expression ◽  
Northern Blotting ◽  
Cell Surface Expression ◽  
Flow Cytometry Analysis ◽  
Hemopoietic Cells ◽  
F Cells ◽  
Class B ◽  
Chicken Mhc ◽  
Hemopoietic Organs

Expression of chicken MHC class (B-F) antigens during ontogeny was determined by binding of anticlass antibody and appearance of B-F transcripts by Northern blotting in chicken organs during embryogenesis until 2 weeks after hatching. MHC class transcripts first become detectable in day 6.5 of embryogenesis. B-F cell-surface expression first becomes detectable in hemopoietic organs by day 10‑12 of embryogenesis and somewhat later in nonhemopoietic organs. Flow cytometry analysis of hemopoietic cells throughout embryogenesis revealed B-Fhi and B-F1 cell populations. The percentage of B-F cells in spleen and bone marrow decreased around hatching, which could reflect either cell flows in these organs during this period or the sensitivity of hemopoietic cells to hatching stress.

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 Cell Surface Expression of Major Histocompatibility Complex Class I Molecules Is Reduced in Hepatitis C Virus Subgenomic Replicon-Expressing Cells

2003 ◽  
Vol 77 (21) ◽  
pp. 11644-11650 ◽  
Author(s):  
Keith D. Tardif ◽  
Aleem Siddiqui
Keyword(s):  
Major Histocompatibility Complex ◽  
Hepatitis C ◽  
Cell Surface ◽  
Mhc Class I ◽  
Surface Expression ◽  
Protein Glycosylation ◽  
Class I ◽  
Cell Surface Expression ◽  
Histocompatibility Complex ◽  
Mhc Class I Molecules

ABSTRACT The hepatitis C virus (HCV) causes chronic hepatitis in most infected individuals by evading host immune defenses. In this investigation, we show that HCV-infected cells may go undetected in the immune system by suppressing major histocompatibility complex (MHC) class I antigen presentation to cytotoxic T lymphocytes. Cells expressing HCV subgenomic replicons have lower MHC class I cell surface expression. This is due to reduced levels of properly folded MHC class I molecules. HCV replicons induce endoplasmic reticulum (ER) stress (K. Tardif, K. Mori, and A. Siddiqui, J. Virol. 76:7453-7459, 2002), which results from a decline in protein glycosylation. Decreasing protein glycosylation can disrupt protein folding, preventing the assembly of MHC class I molecules. This results in the accumulation of unfolded MHC class I. Therefore, the persistence and pathogenesis of HCV may depend upon the ER stress-mediated interference of MHC class I assembly and cell surface expression.

scholarly journals The cationic region from HIV tat enhances the cell-surface expression of epitope/MHC class I complexes

Gene Therapy ◽  
2003 ◽  
Vol 10 (25) ◽  
pp. 2067-2073 ◽  
Author(s):  
J A Leifert ◽  
P D Holler ◽  
S Harkins ◽  
D M Kranz ◽  
J L Whitton
Keyword(s):  
Cell Surface ◽  
Mhc Class I ◽  
Surface Expression ◽  
Class I ◽  
Cell Surface Expression ◽  
Hiv Tat

scholarly journals E3/19K from adenovirus 2 is an immunosubversive protein that binds to a structural motif regulating the intracellular transport of major histocompatibility complex class I proteins.

1990 ◽  
Vol 172 (6) ◽  
pp. 1653-1664 ◽  
Author(s):  
W A Jefferies ◽  
H G Burgert
Keyword(s):  
Major Histocompatibility Complex ◽  
Cell Surface ◽  
Mhc Class I ◽  
Intracellular Transport ◽  
Surface Expression ◽  
Class I ◽  
Cell Surface Expression ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Mhc Class I Molecules

We have previously expressed in transgenic mice a chimeric H-2Kd/Kk protein called C31, which contains the extracellular alpha 1 domain of Kd, whereas the rest of the molecule is of Kk origin. This molecule functions as a restriction element for alloreactive and influenza A-specific cytotoxic T lymphocytes (CTL) but is only weakly expressed at the cell surface of splenocytes. Here, we show that the low cell surface expression is the result of slow intracellular transport and processing of the C31 protein. A set of hybrid molecules between Kd and Kk were used to localize the regions in major histocompatibility complex (MHC) molecules that are important for their intracellular transport and to further localize the structures responsible for binding to the adenovirus 2 E3/19K protein. This protein appears to be an important mediator of adenovirus persistence. It acts by binding to the immaturely glycosylated forms of MHC class I proteins in the endoplasmic reticulum (ER), preventing their passage to the cell surface and thereby reducing the recognition of infected cells by virus-specific T cells. We find the surprising result that intracellular transport and E3/19K binding are controlled primarily by the first half of the second domain of Kd, thus localizing these phenomena to the five polymorphic residues in this region of the Kd protein. This result implies that the E3/19K protein may act by inhibiting peptide binding or by disrupting the oligomerization of MHC class I molecules required for transport out of the ER. Alternatively, the E3/19K protein may inhibit the function of a positively acting transport molecule necessary for cell surface expression of MHC class I molecules.

scholarly journals Chlamydia trachomatisImmune Evasion via Downregulation of MHC Class I Surface Expression Involves Direct and Indirect Mechanisms

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Joyce A. Ibana ◽  
Danny J. Schust ◽  
Jun Sugimoto ◽  
Takeshi Nagamatsu ◽  
Sheila J. Greene ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Surface Expression ◽  
Class I ◽  
Cell Surface Expression ◽  
Class I Mhc ◽  
Pathogen Entry ◽  
Antigen Presenting ◽  
Immune Detection

GenitalC. trachomatisinfections typically last for many months in women. This has been attributed to several strategies by whichC. trachomatisevades immune detection, including well-described methods by whichC. trachomatisdecreases the cell surface expression of the antigen presenting molecules major histocompatibility complex (MHC) class I, MHC class II, and CD1d in infected genital epithelial cells. We have harnessed new methods that allow for separate evaluation of infected and uninfected cells within a mixed population of chlamydia-infected endocervical epithelial cells to demonstrate that MHC class I downregulation in the presence ofC. trachomatisis mediated by direct and indirect (soluble) factors. Such indirect mechanisms may aid in priming surrounding cells for more rapid immune evasion upon pathogen entry and help promote unfettered spread ofC. trachomatisgenital infections.

scholarly journals Binding of Escherichia coli adhesin AfaE to CD55 triggers cell-surface expression of the MHC class I-related molecule MICA

2002 ◽  
Vol 99 (5) ◽  
pp. 2977-2982 ◽  
Author(s):  
V. Tieng ◽  
C. Le Bouguenec ◽  
L. du Merle ◽  
P. Bertheau ◽  
P. Desreumaux ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Surface ◽  
Mhc Class I ◽  
Surface Expression ◽  
Class I ◽  
Cell Surface Expression ◽  
Related Molecule
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