Kaplan State College

Barbara L. F. Kaplan, Ph.D. Assistant Professor
Department of Basic Sciences
Center for Environmental Health Sciences

Contact Information

Education

  • B.S., Environmental Toxicology
    University of California, Davis
  • Ph.D., Pharmacology and Toxicology
    Michigan State University
  • Postdoctoral Research Associate
    University of Chicago

Research Interests

The focus of my laboratory is to elucidate the mechanisms by which cannabinoid compounds (i.e., those derived from marijuana) alter immune function. Previously we demonstrated that plant-derived cannabinoid compounds suppress T cell-dependent humoral immunity. The mechanism by which this occurs likely involves direct T and B cell effects, in addition to disruption of proteins that mediate T cell-B cell interactions. Interestingly, suppression of T cell function does not occur via either of the currently cloned cannabinoid receptors, CB1 or CB2, but suppression of B cell function is mediated through CB1 and/or CB2.

I am currently focusing on two projects. First, I am characterizing the mechanisms by which plant-derived compounds alter T cell function. Although many reports demonstrate that cannabinoid compounds suppress immune function, there are also reports of cannabinoid-mediated enhancement of immune function. These differential effects, at least in T cells, are related to the magnitude to which the T cells are activated with antigen or other agents. Specifically, we demonstrated that cannabidiol (CBD) and D9-tetrahydrocannabinol (D9-THC) enhance or suppress cytokine production and transcription factor activity in response to suboptimal or optimal cellular activation, respectively. These results suggest that caution should be exercised when using cannabinoids therapeutically to suppress immune function since there are conditions under which they produce the opposite effect.

Second, I am examining the role of CB1 and CB2 in cannabinoid-mediated suppression of B cell function. Two different model systems are being utilized for these studies. The first model is a mouse-adapted influenza strain, A/PR8/34. This model can be used to induce flu-specific T cell and B cell responses and can be used to examine the effects of cannabinoids on vaccination. The second model is the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS). Cannabinoids are currently used for effective control of spasticity associated with MS in some countries, although the contribution that cannabinoid-mediated suppression of B cell function makes to cannabinoid MS therapies is not understood.

Recent Publications:

Kaplan BLF, Li J, LaPres JJ, Pruett SB and Karmaus PWF. 2015. Contributions of Non-hematopoietic Cells and Mediators to Immune Responses: Implications for Immunotoxicology. Toxicol Sci. 145: 214-232.

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