Fas ligand breaks tolerance to self-antigens and induces tumor immunity mediated by antibodies

Simon, Anna Katharina, Gallimore, Awen Myfanwy ORCID: https://orcid.org/0000-0001-6675-7004, Jones, Emma, Sawitzki, Birgit, Cerundolo, Vincenzo and Screaton, Gavin R. 2002. Fas ligand breaks tolerance to self-antigens and induces tumor immunity mediated by antibodies. Cancer Cell 2 (4) , pp. 315-322. 10.1016/S1535-6108(02)00151-4

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Abstract

The role of Fas ligand (FasL) in programmed cell death via interaction with its receptor Fas is well characterized. It has been proposed that expression of FasL can confer immune privilege to some organs, allowing them to kill infiltrating lymphocytes and inflammatory cells. However, a number of studies have shown that when tumors or transplants express FasL, rejection often occurs as a consequence of proinflammatory functions of FasL. Here we demonstrate that FasL elicits tumor immunity in a murine melanoma model with weak immunogenicity and low expression of major histocompatibility complex (MHC) class I. We show that protected mice recognize melanocyte differentiation self-antigens. Importantly, tumor immunity is mediated by antibodies, as it can be transferred by serum from protected mice.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine Systems Immunity Research Institute (SIURI)
Subjects:	R Medicine > R Medicine (General)
ISSN:	1535-6108
Last Modified:	17 Oct 2022 08:30
URI:	https://orca.cardiff.ac.uk/id/eprint/309

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