Daniel Kaplan, MD, PhD

Dr. Kaplan is a practicing Dermatologist and leads an active basic research laboratory that focuses on the mechanisms that drive skin inflammation.  As part of that, work his laboratory develops novel tools that allow him to examine the specific functions of skin-resident immune cells.  The lab-engineered mice that selectively lack Langerhans cells.  Contrary to conventional wisdom, these cells were not required for many skin immune responses but rather suppressed cutaneous immune responses leading to a major shift in the understanding of these cells.  The lab also developed a novel skin infection model using C. albicans that allow for detailed interrogation of skin immune responses.  Using this model, Langerhans cells were required for Th17 responses and dendritic cells in the dermis were required for Th1 responses.  Unexpectedly, Th17 responses provided skin protection while Th1 responses provided systemic protection thus revealing a compartmentalization of adaptive responses.  The lab also examines the innate immune response to C. albicans revealing that pain-sensing nerves in the skin directly recognize C. albicans and are required for a cascade of inflammatory events that mediate host defense. This finding is highly significant as it demonstrates that nerves in the skin are major modulators of immune responses, a very novel finding.  The lab has also found that keratinocytes determine whether immune cells can persist in the skin through a novel mechanism of transactivation of TGFb.  Currently, the lab is focused on how individual subsets of cutaneous immune cells work in concert to direct immune responses, how non-immune cells such as nerves and keratinocytes also play critical roles in directing skin immunity, and how each of these pathways can be therapeutically targeted to modify disease processes.