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Department of Internal Medicine

Rheumatology Faculty


John Colgan, Ph.D.
Assistant Professor

Dr. Colgan's research is directed toward understanding both natural and drug-induced mechanisms that suppress immune responses. Recent work has focused on the role of the peptidyl-prolyl isomerase Cyclophilin A (CypA) in the regulation of T helper cell function. CypA has several interesting properties: it is a highly conserved enzyme that may regulate protein conformation, it has an important but poorly understood role in the life cycle of HIV-1, and is a putative receptor for the immunosuppressive drug cyclosporine. Mice lacking CypA develop an allergic disease that seems to be driven by dysregulation of the tyrosine kinase Itk, a key regulator of intracellular signaling pathways in T cells. Molecular analysis shows that CypA functions to repress Itk. Current work is focused on understanding how CypA affects interactions between Itk and its regulatory targets. Mice lacking CypA are also resistant to immunosuppression by cyclosporine, a drug widely used to prevent organ transplant rejection. This property is being exploited to define the cellular and molecular targets of cyclosporine. In another line of investigation, the role of a newly identified class of CD8 + suppressor T cells in controlling autoimmune diabetes is being explored.

John Colgan photo

Graduate School:
Columbia University

Postdoctoral Training:
Columbia University College of Physicians and Surgeons

Honors, Awards, and Organizations

  • NIH Postdoctoral Fellowship
  • Aaron Diamond Foundation for AIDS Research Postdoctoral Fellowship
  • Peter Sajovic Memorial Award for Outstanding Graduate Study in Biology, Columbia University
  • Matilda Woodard Alumni Fellowship, Columbia University
  • American Association for the Advancement of Science
  • American Association of Immunologists
  • American Academy of Allergy, Asthma and Immunology

Recent Publications

  1. Bisikirska, B., Colgan, J., Luban, J., Bluestone, J., and Herold, K.C. Human T cell receptor signaling with modified anti-CD3 monoclonal antibody expands CD8 + T cells and induces regulatory CD8 + CD25 + cells. Submitted.
  2. Chen, Y., Yan, S.S., Colgan, J., Zhang, H.-P., Luban, J., Schmidt, A.M., Stern, D. and Herold, K.C. (2004) Blockade of late stages of autoimmune diabetes by inhibition of the receptor for advanced glycation endproducts (RAGE). J. Immunol. 173: 1399-1405.
  3. Colgan, J., Asmal, M., Yu, B., and Luban, J. Cyclophilin A-deficient mice are resistant to immunosuppression by cyclosporine. Submitted.
  4. Colgan J., Asmal, M., Neagu, M., Yu, B., Schneidkraut, J., Lee, Y., Sokolskaja, E., Andreotti, A.H., and Luban, J. (2004) Cyclophilin A regulates TCR signal strength in CD4 + T cells via a proline-directed conformational switch in Itk. Immunity 21: 189-201.

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