- Postdoc, Yale University School of Medicine
- Residency in Dermatology, Yale University School of Medicine
- M.D./Ph.D., Washington University, St. Louis, MO
Education & Training
1. Hirai, T., Y. Zenke, Y. Yang, L. Bartholin, L. K. Beura, D. Masopust, and D. H. Kaplan. 2019. Keratinocyte-Mediated Activation of the Cytokine TGF-β Maintains Skin Recirculating Memory CD8+ T Cells. Immunity 50: 1249-1261.e5.
2. Cohen, J. A., T. N. Edwards, A. W. Liu, T. Hirai, M. R. Jones, J. Wu, Y. Li, S. Zhang, J. Ho, B. M. Davis, K. M. Albers, and D. H. Kaplan. 2019. Cutaneous TRPV1+ Neurons Trigger Protective Innate Type 17 Anticipatory Immunity. Cell 178: 919-932.e14.
3. Hirai, T., Y. Yang, Y. Zenke, H. Li, V. K. Chaudhri, J. S. D. L. C. Diaz, P. Y. Zhou, B. A.-T. Nguyen, L. Bartholin, C. J. Workman, D. W. Griggs, D. A. A. Vignali, H. Singh, D. Masopust, and D. H. Kaplan. 2021. Competition for Active TGFβ Cytokine Allows for Selective Retention of Antigen-Specific Tissue- Resident Memory T Cells in the Epidermal Niche. Immunity 54: 84-98.e5.
4. Zhang, S., T. N. Edwards, V. K. Chaudhri, J. Wu, J. A. Cohen, T. Hirai, N. Rittenhouse, E. G. Schmitz, P. Y. Zhou, B. D. McNeil, Y. Yang, H. R. Koerber, T. L. Sumpter, A. C. Poholek, B. M. Davis, K. M. Albers, H. Singh, and D. H. Kaplan. 2021. Nonpeptidergic neurons suppress mast cells via glutamate to maintain skin homeostasis. Cell 184: 2151-2166.e16.
5. Whitley, S. K., M. Li, S. W. Kashem, T. Hirai, B. Z. Igyártó, K. Knizner, J. Ho, L. K. Ferris, C. T. Weaver, D. J. Cua, M. J. McGeachy, and D. H. Kaplan. 2022. Local IL-23 is required for proliferation and retention of skin-resident memory TH17 cells. Sci Immunol 7: eabq3254.
The Kaplan Lab is focused on understanding the cellular immune circuits that define responses to infection or damage and maintain immune homeostasis in peripheral tissue with an emphasis on the skin. Areas of focus include how sensory neurons that trigger pain or itch sensation directly modulate innate and adaptive immune responses in the perturbed state and alter the inflammatory ‘set-point’ in the skin during homeostasis. We are also interested in the formation of resident memory T cells and how tissue-specific factors can determine the fitness of these cells. Our approach employs genetic gain- and loss-of-function murine models with inflammatory or infectious triggers which we combine functional, transcriptomic and spatial techniques to define the response. Key findings are confirmed in human tissues where possible.