Abstract
Abstract Immunogenic Heat Shock Proteins (HSPs) are capable of eliciting potent immune responses against their chaperoned antigens and are being investigated as a potential cancer immunotherapy. HSPs signal through the receptor CD91 on the surface of antigen presenting cells and result in the development of a Th1 immune response. We have previously shown that when antigen load is low, HSPs and CD91 are required to prophylactically immunize against tumor development. Since antigen load is also low during nascent tumor development, we hypothesized that CD91 is critical during tumor immunosurveillance. We induced tumors using methylcholanthrene in CD91fl/flx CD11cCremice as well as CD91fl/fllittermates. Tumors developed more rapidly and at a higher incidence in the CD91fl/flx CD11cCremice as compared to the littermate controls. Additionally, tumors in these animals grew more progressively. We are currently immune-phenotyping the tumors that develop in each cohort at multiple time points to determine how the lack of CD91 on CD11c+ cells influences the immune cell infiltrate. Collectively, our data demonstrate that CD91 is a critical mediator of tumor immuneosurveillance and influences the immune infiltration of developing tumors.
Published Version
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