Adenovirus Inversely Modulates Target Cell Class I MHC Antigen Expression and Sensitivity to Natural Killing1

2015 ◽  
pp. 156-159
Author(s):  
J. R. Dawson ◽  
W. J. Storkus ◽  
E. B. Patterson ◽  
P. Cresswell
Keyword(s):  
Target Cell ◽  
Antigen Expression ◽  
Class I ◽  
Class I Mhc ◽  
Cell Class ◽  
Mhc Antigen

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.

Adenovirus Inversely Modulates Target Cell Class I Antigen Expression and Sensitivity to Natural Killing

1989 ◽  
pp. 152-155
Author(s):  
Walter J. Storkus ◽  
Peter Cresswell ◽  
Eric B. Patterson ◽  
Jeffrey R. Dawson
Keyword(s):  
Target Cell ◽  
Antigen Expression ◽  
Class I ◽  
Natural Killing ◽  
Cell Class

The relationship of class I MHC antigen expression to stage IV-S disease and survival in neuroblastoma

1990 ◽  
Vol 25 (4) ◽  
pp. 381-386 ◽  
Author(s):  
Roly Squire ◽  
Carol L. Fowler ◽  
Stephen P. Brooks ◽  
Gary A. Rich ◽  
Donald R. Cooney
Keyword(s):  
Stage Iv ◽  
Antigen Expression ◽  
Class I ◽  
Class I Mhc ◽  
Relationship Of ◽  
The Relationship ◽  
Mhc Antigen

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

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 N-myc expression switched off and class I human leukocyte antigen expression switched on after somatic cell fusion of neuroblastoma cells.

1990 ◽  
Vol 10 (10) ◽  
pp. 5416-5423 ◽  
Author(s):  
R Versteeg ◽  
C van der Minne ◽  
A Plomp ◽  
A Sijts ◽  
A van Leeuwen ◽  
...  
Keyword(s):  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Human Leukocyte ◽  
Antigen Expression ◽  
Suppressor Gene ◽  
Class I ◽  
Class I Mhc ◽  
Putative Tumor Suppressor Gene ◽  
Myc Oncogene ◽  
Myc Gene

Neuroblastomas often show amplification and high expression of the N-myc oncogene. N-myc expression could be explained as a consequence of gene amplification, but an alternative possibility is that expression primarily results from the inactivation or loss of some factor that normally represses the N-myc gene. To test this idea, we fused N-myc-overexpressing neuroblastoma cell lines with lines that do not express N-myc. In the resulting hybrids, N-myc expression turned out to be switched off, although amplified N-myc copies were still present. This suggests that N-myc overexpression in neuroblastomas results, at least in part, from the inactivation of a suppressor gene that is present in normal cells. In rat neuroblastomas, it has been found that N-myc can switch off class I major histocompatibility complex (MHC) expression. Therefore, we analyzed in our hybrid cells whether suppression of N-myc results in reexpression of human class I MHC genes. Because this was found to be the case, the picture emerges of a hierarchic pathway that connects a putative tumor-suppressor gene with the expression of N-myc and consequently of class I MHC, thus affecting the potential immunogenic properties of neuroblastomas.

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