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Andrew Caton, Ph.D.

Andrew J. Caton, Ph.D.


The Caton Laboratory




About the Scientist

Caton studies the mechanisms that govern the ability of the immune system to react against various pathogens and the failure of these underlying mechanisms in autoimmune diseases such as rheumatoid arthritis and lupus.

Caton first joined The Wistar Institute as an assistant professor in 1984 after finishing his postdoctoral work at the University of Oxford, UK. Caton received a bachelor’s degree in biochemistry from the University of East Anglia, UK, in 1977, and a Ph.D. in virology from the University of Cambridge, in 1980. He is also a professor in the department of microbiology at the University of Pennsylvania.

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The Caton Laboratory

The goal of the Caton laboratory is to understand the regulation of the function of B and T lymphocytes that recognize and eliminate infecting microorganisms while remaining neutral toward the host. They also seek to elucidate the alterations in immune response that can lead to autoimmune diseases, such as rheumatoid arthritis and lupus, and play an important role in cancer.


The Caton laboratory has analyzed in great detail the immune response to influenza virus, developing experimental animal models that express a well-characterized antigen from this virus. This model allows the laboratory to analyze how the immune system recognizes and reacts to the body’s own cells and tissues, and determine how these responses are perturbed and can be manipulated under pathologic conditions.

The laboratory has contributed significantly to discovery of regulatory T cell populations that prevent immune responses to host cells and tissues. The role of these regulatory T cells is still not well understood. The ongoing work in the Caton laboratory continues to produce new insights that may ultimately allow these cells to be exploited diagnostically and therapeutically.

Selected Publications

Weissler, K.A., Garcia, V., Caton, A.J., et al. "Distinct modes of antigen presentation promote the formation, differentiation, and activity of foxp3+ regulatory T cells in vivo." J Immunol. 2015 Apr 15;194(8):3784-97. doi: 10.4049/jimmunol.1402960. Epub 2015 Mar 16.

Wolf, A.I., Strauman, M.C., Mozdzanowska, K., Whittle, J.R., Williams, K.L., Sharpe, A.H., Weiser, J.N., Caton, A.J., Hensley, S.E., Erikson, J. "Coinfection with Streptococcus pneumoniae modulates the B cell response to influenza virus." J Virol. 2014 Oct;88(20):11995-2005. doi: 10.1128/JVI.01833-14. Epub 2014 Aug 6.

Weissler, K.A., Caton, A.J. "The role of T-cell receptor recognition of peptide:MHC complexes in the formation and activity of Foxp3⁺ regulatory T cells." Immunol Rev. 2014 May;259(1):11-22. doi: 10.1111/imr.12177.

Perng, O.A., Aitken, M., Caton, A.J., et al. "The degree of CD4+ T cell autoreactivity determines cellular pathways underlying inflammatory arthritis." J Immunol. 2014 Apr 1;192(7):3043-56. doi: 10.4049/jimmunol.1302528. Epub 2014 Mar 3.

Caton, A.J., Kropf, E., Jordan, M.S., et al. "Strength of TCR signal from self-peptide modulates autoreactive thymocyte deletion and Foxp3(+) Treg-cell formation." Eur J Immunol. 2014 Mar;44(3):785-93. doi: 10.1002/eji.201343767. Epub 2013 Dec 27.

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