Fred Stuart Kantor MD

Paul B. Beeson Professor of Medicine (Immunology); Interim Chief, Section of Clinical Immunology and Allergy

Research Interests

Host parasite relationship in Lyme Borreliosis; immune relationship between Borrelia burgdorferi and the host in chronic infection


Research Summary

We are involved in research involving the host parasite relationship in Lyme Borreliosis. We have two ongoing projects. The first has to do with tick immunity, and to this end we are purifying ticks salivary and mid-gut antigens to determine the nature of the antigenic stimulation that leads to tick immunity and also preparing specific antibodies to screen expression libraries of such antigens. We have developed a system of measuring tick immunity in guinea pigs and apply and test our purified and recombinant antigens in this system.

Our second project involves the immune relationship between Borrelia burgdorferi and the host in chronic infection. We and others have shown that after several days of infection, the spirochetes, Borrelia burgdorferi, are not sensitive to antibodies which would protect a naive animal if they were on board prior to the inoculation of the infecting organisms. We have learned that the organism changes in vitro in response to a non-immune host stimulus. We are currently investigating what is the stimulus or stimuli and how does the organism change? What antigens does it stop producing on its surface and what new antigens are produced in vivo and are these protective in ways different than antigens found in broth grown organisms. Finally, while cell mediated immunity has not been found to be important in the protection of naive hosts from infection with Borrelia burgdorferi, it may well be that cell mediated immunity is effective in clearing the chronically infected host of tissue bound B. burgdorferi. This too is the subject of ongoing investigation.


Selected Publications

  • Thomas MJ, Noble A, Sawicka E, Askenase PW, Kemeny DM. CD8 T cells inhibit IgE via dendritic cell IL-12 induction that promotes Th1 T cell counter-regulation. J Immunol. 2002 Jan 1168(1):216-23.
  • Geba GP, Ptak W, Askenase PW. Topical tacrolimus and cyclosporin A differentially inhibit early and late effector phases of cutaneous delayed-type and immunoglobulin E hypersensitivity. Immunology. 2001 Oct104(2):235-42.
  • Askenase PW. Yes T cells, but three different T cells (alphabeta, gammadelta and NK T cells), and also B-1 cells mediate contact sensitivity. Clin Exp Immunol. 2001 Sep125(3):345-50.
  • Thomas MJ, MacAry PA, Noble A, Askenase PW, Kemeny DM. T cytotoxic 1 and T cytotoxic 2 CD8 T cells both inhibit IgE responses. Int Arch Allergy Immunol. 2001 Jan-Mar124(1-3):187-9.
  • Askenase PW, Tsuji RF. B-1 B cell IgM antibody initiates T cell elicitation of contact sensitivity. Curr Top Microbiol Immunol. 2000252:171-7.

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