Abrogation of tumorigenicity by MHC class II antigen expression requires the cytoplasmic domain of the class II molecule

Transfection of syngeneic MHC class II genes into the lethal mouse SaI tumor abrogates the malignancy of the tumor in the autologous host, and protects the host against subsequent challenges with the wild type class II- tumor. We have hypothesized that the transfectants induce protective immunity by...

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Bibliographic Details
Published inThe Journal of immunology (1950) Vol. 147; no. 7; pp. 2419 - 2422
Main Authors Ostrand-Rosenberg, S, Roby, CA, Clements, VK
Format Journal Article
LanguageEnglish
Published Bethesda, MD Am Assoc Immnol 01.10.1991
American Association of Immunologists
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Summary:Transfection of syngeneic MHC class II genes into the lethal mouse SaI tumor abrogates the malignancy of the tumor in the autologous host, and protects the host against subsequent challenges with the wild type class II- tumor. We have hypothesized that the transfectants induce protective immunity by functioning as APC for tumor peptides, and stimulating tumor-specific Th cells. Recent in vitro studies suggest that Ag presentation by class II-restricted APC requires the cytoplasmic domain of the class II molecule, and may involve intracellular signaling via the cytoplasmic domain. To determine if the class II cytoplasmic domain is required for enhanced tumor-specific immunity, SaI mouse sarcoma cells were transfected with syngeneic Aak and Abk genes with truncated cytoplasmic domains. These transfectants are as malignant as wild type class II- SaI cells in autologous A/J mice. Stimulation of tumor-specific immunity by class II+ tumor cells is therefore dependent on the class II cytoplasmic region, and may involve intracellular signaling events.
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ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.147.7.2419