The Sherman Laboratory

Research Focus

Recognition of Self and Tumor Antigens

Fundamental to the strategy of the immune system is discrimination between self and non-self. This enables the immune system to respond to and eliminate foreign pathogens without harming one's own tissues. Autoimmune disease represents aberrant immune destruction of self-tissue, whereas other diseases such as cancer are, in part, due to immune tolerance of self. One goal of our laboratory is to augment the ability of T lymphocytes to respond to certain self-antigens in order to eliminate tumor cells. To this end, we utilize a variety of transgenic murine models in order to study autoimmunity and tumor immunity. In particular, we are studying how expression of proteins in normal tissues alters immune recognition and responsiveness to antigens of these proteins when they are subsequently encountered on normal tissue or tumor cells. We use similar models to probe defects in immune tolerance that result in autoimmune destruction of pancreatic islets leading to type 1 diabetes.

Selected References

Wei, C.H., and Sherman, L.A.2007. N-Terminal trimer extension of nominal CD8T cell epitopes is sufficient to promote cross-presentation to cognate CD8 T cells in vivo. J. Immunol. 179(12):8280-8286.

Wong, S.B.J., Bos, R., Sherman, L.A. 2008. Tumor specific CD4⁺ T cells render the tumor environment permissive for infiltration by low avidity CD8⁺ T cells. J. Immunol. 180: 3122–3131.

Redmond, W.L., Wei, C.H., Kreuwel, H.T.C., Sherman, L.A. 2008. The apoptotic pathway contributing to the deletion of naïve CD8 T cells during induction of peripheral tolerance to a cross-presented self-antigen. J. Immunol. 180(8):5275-82.

Verdeil, G., Marquardt, K., Surh, C.D., Sherman, L.A. 2008. Adjuvants targeting innate and adaptive immunity synergize to enhance tumor immunotherapy. PNAS. 105(43):16683-8 PMCID: PMC2575480