Immunostimulating Complexes Allow the in vivo Immunisation of Class I MHC-Restricted Murine CD8 + Cytolytic T Lymphocytes towards Soluble Antigens

2015 ◽  
pp. 114-117
Author(s):  
Klaus Heeg ◽  
Hermann Wagner
Keyword(s):  
T Lymphocytes ◽  
Class I ◽  
Cytolytic T Lymphocytes ◽  
Class I Mhc ◽  
Immunostimulating Complexes

Virosome-mediated delivery of protein antigens in vivo: efficient induction of class I MHC-restricted cytotoxic T lymphocyte activity

Vaccine ◽  
2005 ◽  
Vol 23 (10) ◽  
pp. 1232-1241 ◽  
Author(s):  
Laura Bungener ◽  
Anke Huckriede ◽  
Arjan de Mare ◽  
Jacqueline de Vries-Idema ◽  
Jan Wilschut ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
Cytotoxic T Lymphocyte ◽  
Class I ◽  
Protein Antigens ◽  
Class I Mhc ◽  
Efficient Induction ◽  
Lymphocyte Activity

scholarly journals Exogenous Expression of Equine MHC Class I Molecules in Mice Increases Susceptibility to Equine Herpesvirus 1 Pulmonary Infection

2019 ◽  
Vol 56 (5) ◽  
pp. 703-710 ◽  
Author(s):  
Erina Minato ◽  
Keisuke Aoshima ◽  
Atsushi Kobayashi ◽  
Naomi Ohnishi ◽  
Nobuya Sasaki ◽  
...  
Keyword(s):  
Mhc Class I ◽  
Virus Antigen ◽  
Class I ◽  
Equine Herpesvirus ◽  
Class I Mhc ◽  
Equine Herpesvirus 1 ◽  
Exogenous Expression ◽  
Herpesvirus 1 ◽  
Entry Receptor

Equine herpesvirus 1 (EHV-1) uses equine major histocompatibility complex class I (MHC class I) as an entry receptor. Exogenous expression of equine MHC class I genes in murine cell lines confers susceptibility to EHV-1 infection. To examine the in vivo role of equine MHC class I as an entry receptor for EHV-1, we generated transgenic (Tg) mice expressing equine MHC class I under the control of the CAG promoter. Equine MHC class I protein was expressed in the liver, spleen, lung, and brain of Tg mice, which was confirmed by Western blot. However, equine MHC class I antigen was only detected in bronchiolar epithelium and not in other tissues, using the immunofluorescence method employed in this study. Both Tg and wild-type (WT) mice developed pneumonia 3 days after intranasal infection with EHV-1. The bronchiolar epithelial cells of Tg mice showed more severe necrosis, compared with those in WT mice. In addition, the number of virus antigen-positive cells in the lungs was higher in Tg mice than in WT mice. These results suggest that exogenous expression of equine MHC class I renders mice more susceptible to EHV-1 infection.

scholarly journals Targeting mutant p53-expressing tumours with a T cell receptor-like antibody specific for a wild-type antigen

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Lionel Low ◽  
Angeline Goh ◽  
Joanna Koh ◽  
Samantha Lim ◽  
Cheng-I Wang
Keyword(s):  
Cell Receptor ◽  
Class I ◽  
Human Antibody ◽  
Mutant P53 ◽  
Wild Type ◽  
Class I Mhc ◽  
Type Antigen ◽  
Wide Range

AbstractAccumulation of mutant p53 proteins is frequently found in a wide range of cancers. While conventional antibodies fail to target intracellular proteins, proteosomal degradation results in the presentation of p53-derived peptides on the tumour cell surface by class I molecules of the major histocompatibility complex (MHC). Elevated levels of such p53-derived peptide-MHCs on tumour cells potentially differentiate them from healthy tissues. Here, we report the engineering of an affinity-matured human antibody, P1C1TM, specific for the unmutated p53125-134 peptide in complex with the HLA-A24 class I MHC molecule. We show that P1C1TM distinguishes between mutant and wild-type p53 expressing HLA-A24+ cells, and mediates antibody dependent cellular cytotoxicity of mutant p53 expressing cells in vitro. Furthermore, we show that cytotoxic PNU-159682-P1C1TM drug conjugates specifically inhibit growth of mutant p53 expressing cells in vitro and in vivo. Hence, p53-associated peptide-MHCs are attractive targets for the immunotherapy against mutant p53 expressing tumours.

scholarly journals Recognition of interspecies hybrid class I histocompatibility antigens by antigen-specific cytolytic T lymphocytes.

1985 ◽  
Vol 82 (18) ◽  
pp. 6276-6280 ◽  
Author(s):  
R. Maziarz ◽  
H. Allen ◽  
J. L. Strominger ◽  
R. Flavell ◽  
P. A. Biro ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Class I ◽  
Cytolytic T Lymphocytes ◽  
Histocompatibility Antigens ◽  
Hybrid Class ◽  
Interspecies Hybrid

scholarly journals Immunotherapy of a murine tumor with interleukin 2. Increased sensitivity after MHC class I gene transfection.

1987 ◽  
Vol 166 (6) ◽  
pp. 1716-1733 ◽  
Author(s):  
J S Weber ◽  
G Jay ◽  
K Tanaka ◽  
S A Rosenberg
Keyword(s):  
T Cells ◽  
Mhc Class I ◽  
Interleukin 2 ◽  
Class I ◽  
High Dose ◽  
Class I Mhc ◽  
High Doses ◽  
I Gene

We have shown that two weakly immunogenic MCA sarcomas developed in our laboratory that are sensitive to high-dose IL-2 immunotherapy express class I MHC in vivo and in vitro. Two nonimmunogenic MCA sarcomas are relatively insensitive to IL-2 therapy and express minimal or no class I MHC molecules in vivo and in vitro. To study the role of MHC in the therapy of tumors with IL-2, a class I-deficient murine melanoma, B16BL6, was transfected with the Kb class I gene. Expression of class I MHC rendered B16BL6 advanced pulmonary macrometastases sensitive to IL-2 immunotherapy. 3-d micrometastases of CL8-2, a class I transfected clone of B16BL6, were significantly more sensitive to IL-2 therapy than a control nontransfected line. Expression of Iak, a class II MHC molecule, had no effect on IL-2 therapy of transfectant pulmonary micrometastases in F1 mice. By using lymphocyte subset depletion with mAbs directed against Lyt-2, therapy of class I transfectant macrometastases with high-dose IL-2 was shown to involve an Lyt-2 cell. In contrast, regression of micrometastases treated with low-dose IL-2 involved Lyt-2+ cells, but regression mediated by high doses of IL-2 did not. We hypothesize that both LAK and Lyt-2+ T cells effect IL-2-mediated elimination of micrometastases, but only Lyt-2+ T cells are involved in macrometastatic regression. Low doses of IL-2 stimulate Lyt-2+ cells to eliminate class I-expressing micrometastases, but high doses of IL-2 can recruit LAK cells to mediate regression of micrometastases independent of class I expression. Only high-dose IL-2, mediating its effect predominantly via Lyt-2+ cells, is capable of impacting on MHC class I-expressing macrometastases. Macrometastases devoid of class I MHC antigens appear to be resistant to IL-2 therapy.

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