Andrew J. Caton, Ph.D.
Andrew J. Caton, Ph.D.
- Professor, Tumor Microenvironment and Metastasis Program
- Member, Vaccine Center
- 215-898-3871, Office
The aim of the Caton laboratory is to illuminate the mechanisms that govern the ability of the immune system to react against various pathogens. In striving to define how these key mechanisms are regulated, the Caton laboratory also seeks to understand 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 from the University of East Anglia, UK in biochemistry in 1977, and his Ph.D. from the University of Cambridge in virology in 1980. He is also the Wistar Professor in the department of microbiology at the University of Pennsylvania.
The goal of the Caton laboratory is to define how B cells and T cells, lymphocytes that recognize and eliminate infecting microorganisms while remaining neutral toward the host, are regulated, and to understand the changes in immune response that can lead to autoimmune diseases such as rheumatoid arthritis and lupus, and can also play an important role in cancer. In particular, the laboratory has analyzed immune response to influenza virus in great detail, developing experimental animal models that express a well-characterized antigen from the influenza virus as one of the mouse’s own proteins. This approach is allowing 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 Caton laboratory has contributed significantly to the recent interest in the role that regulatory T cells can play in preventing autoimmunity, and helped establish the existence of cell populations that prevent immune responses to host cells and tissues. How these regulatory T cells affect immune responses in general, and an autoimmune disease like rheumatoid arthritis, in particular, is not well understood. The on-going work of the Caton laboratory continues to produce new insights that may one day allow these cells to be exploited diagnostically and therapeutically.
1. Jordan, M.S., Boesteanu, A., Reed, A.J., Petrone, A.L., Holenbeck, A.E., Lerman, M.A., Naji, A., Caton, A.J.: Thymic selection of CD4+CD25+ regulatory T cells induced by an agonist self-peptide. Nat Immunol 2:301-306, 2001. PMID: 11276200
2. Seo, S.J., Fields, M.L., Buckler, J.L., Reed, A.J., Mandik-Nayak, L., Nish, S.A., Noelle, R.J., Turka, L.A., Finkelman, F.D., Caton, A.J., Erikson, J.: The impact of T helper and T regulatory cells on the regulation of anti-double-stranded DNA B cells. Immunity 16:535-546, 2002. PMID: 11970877
3. Guay, H.M., Larkin III, J., Cozzo Picca, C., Panarey, L. and Caton, A.J. High frequencies of autoreactive CD4+ T cells can drive autoreactive memory B cell formation. J. Immunol. 178: 4793-4802, 2007. PMID: 17404260
4. Rankin, A.L., Reed, A.J., Oh, S., Cozzo Picca, C., Guay, H.M., Larkin, J., 3rd, Panarey, L., Aitken, M.K., Koeberlein, B., Lipsky, P.E., Tomaszewski, J.E., Naji, A. and Caton, A.J. CD4+ T cells recognizing a single self-peptide expressed by APCs induce spontaneous autoimmune arthritis. J Immunol 180: 833-841. PMID: 18178822
5. Picca, C.C., Oh, S., Panarey, L., Aitken, M., Basehoar, A. and Caton, A.J.Thymocyte deletion can bias Treg formation toward low-abundance self-peptide. Eur J Immunol, 39: 3301-6, 2009. PMID: 19768697
6. Oh, S., Rankin, A.L. and Caton, A.J.CD4+CD25+ regulatory T cells in autoimmune arthritis. Immunol Rev. 233: 97-111, 2010. PMID: 20192995
7. Simons DM, Picca CC, Oh S, Perng OA, Aitken M, Erikson J, Caton AJ. How specificity for self-peptides shapes the development and function of regulatory T cells. J. Leuk. Biol. 88: 1099-1107, 2010. PMID: 20495071
8. Feng, X., Ippolito, G.C., Tian, L., Wiehagen, K., Oh, S., Sambandam, A., Willen, J., Bunte, R.M., Maika, S.D., Harriss, J.V., Caton, A.J., Bhandoola, A., Tucker, P.W. and Hu, H. Foxp1 is an essential transcriptional regulator for the generation of quiescent naive T cells during thymocyte development. Blood, 115: 510-518, 2010. PMID: 19965654
9. Wolf AI, Mozdzanowska K, J Quinn W 3rd, Metzgar M, Williams KL, Caton AJ, Meffre E, Bram RJ, Erickson LD, Allman D, Cancro MP, Erikson J. Protective antiviral antibody responses in a mouse model of influenza virus infection require TACI. J Clin Invest. 121: 3954-3964, 2011 PMID: 21881204
10. Cozzo Picca C, Simons DM, Oh S, Aitken M, Perng OA, Mergenthaler C, Kropf E, Erikson J, and Caton AJ. CD4+CD25+Foxp3+ regulatory T cell formation requires more specific recognition of a self-peptide than thymocyte deletion. Proc Natl Acad Sci U S A, 108: 14890-14895, 2011 PMID: 21873239
11. Oh S, Aitken M, Simons DM, Basehoar A, Garcia V, Kropf E, and Caton AJ. Requirement for diverse TCR specificities determines regulatory T cell activity in a mouse model of autoimmune arthritis. J. Immunol. 188: 4171-4180, 2012. PMID: 22450809
12. Simons, DM, Oh, S, Kropf, E, Aitken, M, Garcia, V, Basegoar, A, and Caton AJ. Autoreactive Th1 cells activate monocytes to support regional Th17 cell responses in inflammatory arthritis. J. Immunol. 190, 3134-3141, 2013. PMID: 23420889
13. Bedoya F, Cheng G-S, Leibow A, Zakhary N, Weissler K, Garcia V, Aitken M, Kropf E, Garlick DS, Wherry JE, Erikson J, Caton AJ. 2013. Viral antigen induces differentiation of Foxp3+ natural regulatory T cells in influenza virus-infected mice. J Immunol, 190: 6115-6125, 2013. PMID: 23667113