Leishmaniasis:

Visceral Leishmaniasis: Immunoregulation of Host Response to Antileishmanial Chemotherapy and Immunochemotherapy. Murray. Various host immunologic mechanisms, largely T [Th1] cell-dependent, regulate the in vivo capacity to respond to antileishmanial chemotherapy. Using pentavalent antimony and amphotericin B as two distinct pharmacologic probes in L. donovani-infected mice, this project is examining the host mechanisms that determine or can enhance initial in vivo host responsiveness to chemotherapy and/or regulate subsequent prevention of posttreatment relapse. The work is focused on the interaction of antileishmanial chemotherapy with amplified cytokine-induced macrophage activation, chemokine-induced granuloma assembly, CD4 and CD8 cell responses, activating and deactivating mechanisms (cytokines, receptors, intracellular signaling) and immunologic effects induced by chemotherapy itself. The goal of the project is to employ immunochemotherapy to improve treatment-induced outcome in visceral leishmaniasis, both the initial host response to chemotherapy and the long-term prevention of relapse in this intracellular protozoal infection.

  • Murray HW. Accelerated control of visceral Leishmania donovani infection in IL-6-/- mice. Infect Immun 2008;76:4088-91.
  • Murray HW, Tsai CW, Liu J, Ma X. Responses to Leishmania donovani in mice deficient in IL-12, IL-12/IL-23 or IL-18. Infect Immun 2006; 74:4370-74.
  • Murray HW, Tsai CW, Liu J, Ma X. Visceral Leishmania donovani infection in IL13-/- mice. Infect Immun 2006; 74:2487-90.
  • Murray HW, Xiang Z, Ma X. Responses to Leishmania donovani in mice deficient in both phagocyte oxidase and inducible nitric oxide synthase. Am J Trop Med Hyg 2006; 74:1013-15.


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Infectious Diseases
Roy M. Gulick, MD, Chief

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Tel: (212) 746-4914
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