Class I MHC Antigen Processing

2006 ◽  
pp. 1-30
Author(s):  
Peter J. Miller ◽  
Edward J. Collins
Keyword(s):  
Antigen Processing ◽  
Class I ◽  
Class I Mhc ◽  
Mhc Antigen

scholarly journals Inhibition by Woodchuck Hepatitis Virus of Class I Major Histocompatibility Complex Presentation on Hepatocytes Is Mediated by Virus Envelope Pre-S2 Protein and Can Be Reversed by Treatment with Gamma Interferon

2006 ◽  
Vol 80 (17) ◽  
pp. 8541-8553 ◽  
Author(s):  
Jinguo Wang ◽  
Tomasz I. Michalak
Keyword(s):  
Major Histocompatibility Complex ◽  
Antigen Processing ◽  
Hepatitis Virus ◽  
Gamma Interferon ◽  
Class I ◽  
Woodchuck Hepatitis Virus ◽  
Major Histocompatibility ◽  
Class I Mhc ◽  
Histocompatibility Complex ◽  
Mhc Antigen

ABSTRACT Presentation of class I major histocompatibility complex (MHC) is severely down-regulated on hepatocytes in chronic hepatitis caused by woodchuck hepatitis virus (WHV). To determine which of the viral proteins mediates class I MHC antigen suppression, cultured normal woodchuck hepatocytes were transfected with the complete WHV genome, sequences encoding individual virus proteins, or whole virus genomes in which transcription of selected proteins was disabled by site-specific mutagenesis. It was found that hepatocyte presentation of class I MHC antigen was significantly inhibited following transfection with complete WHV genome or with viral subgenomic fragments encoding envelope pre-S2 protein or pre-S1 protein, which naturally encompasses pre-S2 amino acid sequence. In contrast, hepatocytes transfected with WHV X gene alone demonstrated a profound enhancement in the class I antigen display, whereas those expressing virus major S protein or nucleocapsid (core) protein were not different from control hepatocytes. Analysis of the mutated WHV sequences confirmed that the envelope pre-S2 protein was responsible for inhibition of the class I MHC antigen display. Interestingly, treatment with recombinant woodchuck gamma interferon (rwIFN-γ) restored the inhibited presentation of the class I antigen. Moreover, the class I antigen suppression was not associated with down-regulation of hepatocyte genes for class I MHC heavy chain, β2-microglobulin, transporters associated with antigen processing, and proteasome subunits. These findings indicate that the defective presentation of class I MHC antigen on hepatocytes transcribing WHV is a consequence of posttranscriptional suppression exerted by virus pre-S2 protein and that this hindrance can be fully reversed by IFN-γ.

Identification of MHC-I Accessible Proteins from Salmonella Typhimurium

2001 ◽  
Vol 7 (S2) ◽  
pp. 616-617
Author(s):  
D. Ellefson ◽  
D. Parker ◽  
F. Heffron
Keyword(s):  
Salmonella Typhimurium ◽  
Host Cell ◽  
Antigen Processing ◽  
Bacterial Pathogens ◽  
Immune Surveillance ◽  
Class I ◽  
Whole Genome Analysis ◽  
Class I Mhc ◽  
Mhc I ◽  
Host Interaction

Intracellular bacterial pathogens such as Salmonella typhimurium secrete proteins into the host cell after infection. These proteins alter the normal structural and metabolic machinery of the host cell and benefit the bacterium by facilitating replication and avoidance of host immune surveillance. Since the host cytoplasmic localization of these proteins infers access to the class-I MHC antigen processing and presentation machinery of the host cell, we collectively refer to these proteins as Class- I Accessible Proteins (CAPs).The design of vaccines for new and emerging bacterial pathogens is often constrained by the selection of appropriate and specific antigens. While vaccine design is being greatly aided by whole genome analysis of bacterial pathogens, it has been of limited use in the assignment of function and host subcellular localization of a large percentage of bacterial proteins. in addition, analysis of the bacteria/host interaction is further complicated by the complex lifestyle of the pathogen.

Transport and Expression of Class I MHC Glycoproteins in an Antigen-processing Mutant Cell Line

1992 ◽  
Vol 57 (0) ◽  
pp. 571-577 ◽  
Author(s):  
E.-M. Click ◽  
K.S. Anderson ◽  
M.J. Androlewicz ◽  
M.L. Wei ◽  
P. Cresswell
Keyword(s):  
Cell Line ◽  
Antigen Processing ◽  
Mutant Cell ◽  
Class I ◽  
Class I Mhc ◽  
Mutant Cell Line

Role of Class-II Major Histocompatibility Complex (MHC)-Antigen–Positive Donor Leukocytes in Transfusion-Induced Alloimmunization to Donor Class-I MHC Antigens

Blood ◽  
1998 ◽  
Vol 92 (2) ◽  
pp. 690-694
Author(s):  
K.J. Kao ◽  
M.L.U. del Rosario
Keyword(s):  
Immune Response ◽  
Peripheral Blood ◽  
Class Ii ◽  
Class I ◽  
Mononuclear Leukocytes ◽  
Class I Mhc ◽  
Mhc Antigens ◽  
Mhc Molecules ◽  
Class Ii Mhc ◽  
Mhc Antigen

It has been shown that peripheral-blood mononuclear leukocytes (MNL) are responsible for transfusion-induced alloimmunization to donor major histocompatability complex (MHC) antigens. However, it is not known which subset of MNL is responsible for this immune response. Because elimination of class-II MHC antigen-positive passenger leukocytes effectively prolongs the survival of allografts, it has been hypothesized that class-II positive MNL are responsible for immunizing transfusion recipients to donor MHC antigens. To test this hypothesis, two different approaches were used. First, we compared the alloantigenicity of BALB/c mice (H-2d) peripheral blood MNL before and after depletion of class-II positive cells. CBA mice (H-2k) were used as transfusion recipients. Antibody development to donor class-I H-2 antigens was determined by flow cytometry and enzyme-linked immunoassay. After four weekly transfusions of MNL depleted for class-II positive cells, only 25% of recipient mice developed antibodies to donor H-2d antigens. In contrast, all mice transfused with control MNL became immunized. Second, we studied the alloantigenicity of peripheral MNL from C57BL/6 mice (H-2b) with homozygous deficiency of class-II MHC molecules in H-2 disparate recipient mice. After transfusions with class-II MHC molecule-deficient MNL, 0% of BALB/c, 40% of C57BR, and 25% of CBA-recipient mice developed antibodies to donor H-2b antigen. All control recipient mice were immunized. The antibody activities of the controls were also higher than those in the treatment group who became immunized. Thus, our study shows that class-II MHC antigen-positive MNL play a significant role in transfusion-induced alloimmunization to donor class-I MHC antigens. The results also support the hypothesis that direct antigen presentation by donor class-II positive MNL to the immune system of transfusion recipients is critical for the initiation of humoral immune response to donor MHC antigens.

Induction of Tolerance Toward Rat Cardiac Allografts by Treatment With Allochimeric Class I MHC Antigen And FTY7201

1997 ◽  
Vol 64 (10) ◽  
pp. 1407-1414 ◽  
Author(s):  
Shih-Chieh Chueh ◽  
Ling Tian ◽  
Min Wang ◽  
Mou-Er Wang ◽  
Stanislaw M. Stepkowski ◽  
...  
Keyword(s):  
Class I ◽  
Class I Mhc ◽  
Cardiac Allografts ◽  
Mhc Antigen ◽  
Induction Of Tolerance

scholarly journals Depletion of CD8+ cells in human thymic medulla results in selective immune deficiency.

1989 ◽  
Vol 170 (6) ◽  
pp. 2177-2182 ◽  
Author(s):  
C M Roifman ◽  
D Hummel ◽  
H Martinez-Valdez ◽  
P Thorner ◽  
P J Doherty ◽  
...  
Keyword(s):  
T Cells ◽  
Peripheral Blood ◽  
Inbred Mice ◽  
Pneumocystis Carinii ◽  
Antigen Expression ◽  
Class I ◽  
Class I Mhc ◽  
Cd8 Cells ◽  
Mhc Antigen ◽  
Selection Of

CD8 molecules expressed on the surface of a subset of T cells participate in the selection of class I MHC antigen-restricted T cells in the thymus, and in MHC-restricted immune responses of mature class I MHC antigen-restricted T cells. Here we describe an immune-deficient patient with lack of CD8+ peripheral blood cells. The patient presented with Pneumocystis carinii pneumonia and was unable to reject an allogeneic skin graft, but had normal primary and secondary antibody responses. Examination of the patient's thymus revealed that the loss of CD8+ cells occurred during intrathymic differentiation: the patient's immature cortical thymocytes included both CD4+ and CD8+ cells while the mature medullary cells expressed the CD4 but not the CD8 protein on their surface. Northern blot and polymerase chain reaction analyses revealed the presence of CD8 alpha and beta mRNA in the patient's thymus but not in the peripheral blood. Both class I MHC antigen expression and the expressed TCR V beta repertoire are normal in this patient. These data are consistent with an impaired selection of CD8+ cells in the patient's thymus and support the role of the CD8 surface protein in thymic selection previously characterized in genetically manipulated and inbred mice.

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