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NAME Yasuhiro Suzuki, Ph.D., D.M.Sc. |
POSITION TITLE Associate Professor |
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EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, and include postdoctoral training.) |
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INSTITUTION AND LOCATION |
DEGREE (if applicable) |
YEAR(s) |
FIELD OF STUDY |
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University of Tokyo, Tokyo, Japan |
B.S. |
1976 |
Pharmaceutical Sciences |
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University of Tokyo, Tokyo, Japan |
Ph.D. |
1982 |
Microbiol. & Immunol. |
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Jikei University, Tokyo, Japan |
D.M.Sc. |
1989 |
Infection immunity |
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Positions and Employment
1976-1986 Research Associate, Department of Parasitology, Jikei University School of Medicine, Tokyo, Japan
1986-1988 Visiting Scientist, Division of Infectious Diseases, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA
1988-1993 Assistant Professor, Department of Parasitology, Jikei University School of Medicine, Tokyo, Japan
1993-1994 Research Associate, Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA, and Senior Research Associate, Research Institute, Palo Alto Medical Foundation, Palo Alto, CA, USA
1998-2001 Consulting Assistant Professor, Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA, and Senior Research Associate, Research Institute, Palo Alto Medical Foundation, Palo Alto, CA, USA
Honors
2002
WVTF Researcher of
the Week
My laboratory has been investigating the mechanism of host-pathogen interactions in infection with Toxoplasma gondii, an obligate intracellular protozoan parasite. Our recent focus of research is the molecular immunopathogenesis of cerebral toxoplasmosis. Toxoplasmic encephalitis (TE) has been a major opportunistic infectious disease in immunocompromised patients, such as those with AIDS and organ transplant recipients. In addition, TE is an excellent model for analyzing the mechanism of host defense in the brain. We have developed murine models of TE and found three factors critical for determining the host resistance to this disease. These are: IFN-g-mediated immune response, the genetic background of the host, and the strain of T. gondii. We are trying to obtain understanding of the molecular basis of host resistance to development of TE, by defining how the IFN-g-mediated immune response functions in the brain and how the genetic background of the host and the strain of T. gondii affect the immune response.
(Publications selected from over 100 publications).
Suzuki Y, Orellana MA, Schreiber RD and Remington JS. Interferon-g: The major mediator of resistance against Toxoplasma gondii. Science 240:516-518, 1988.
Suzuki Y and Remington JS. Dual regulation of resistance against Toxoplasma gondii infection by Lyt- 2+ and Lyt-1+, L3T3+ T cells in mice. J Immunol 140:3943-3946, 1988.
Suzuki Y, Conley FK, Remington JS. Importance of endogenous IFN-g for prevention of toxoplasmic encephalitis in mice. J Immunol 142:954-958, 1989.
Suzuki Y, Conley FK and Remington JS. Differences in virulence and development of encephalitis during chronic infection vary with the strain of Toxoplasma gondii. J Infect Dis 159:790-794, 1989.
Suzuki Y and Remington JS. The effect of anti-IFN-g antibody on the protective effect of Lyt-2+ immune T cells against toxoplasmosis in mice. J Immunol 144(5):1954-1956, 1990.
Suzuki Y, Conley FK and Remington JS. Treatment of toxoplasmic encephalitis in mice with recombinant gamma interferon. Infect Immun 58(9):3050-3055, 1990.
Suzuki Y, Joh K and Kobayshi A. Tumor necrosis factor-independent protective effect of recombinant IFN-g against acute toxoplasmosis in T cell-deficient mice. J Immunol 147:2728-2733, 1991.
Suzuki Y, Joh K, Orellana MA, Conley FK and Remington JS. A gene(s) within the H-2D region determines the development of toxoplasmic encephalitis in mice. Immunology 74(4):732-739, 1991.
Suzuki Y and Remington JS. In: Encyclopedia of Immunology, Raitt IM and Delves PJ eds. Academic Press, pp 1495-1496, 1992.
Suzuki Y, Orellana MA, Wong SY, Conley FK and Remington JS. Susceptibility to chronic infection with Toxoplasma gondii does not correlate with susceptibility to acute infection in mice. Infect Immun 61:2284-2288, 1993.
Watanabe H, Suzuki Y, Makino M and Fujiwara M. Toxoplasma gondii: Induction of toxoplasmic encephalitis in mice with chronic infection by inoculation of a murine leukemia virus inducing immunodeficiency. Exp Parasitol 76:39-45, 1993.
Suzuki Y, Joh K, Kwon O-C, Yang Q, Conley FK and Remington JS. A gene(s) in the D/L region of the MHC class I antigens but not TNF-a gene determines development of toxoplasmic encephalitis in mice. J Immunol 153:4649-4654, 1994.
Suzuki Y, Yang Q and Remington JS. Genetic resistance against toxoplasmosis depends on the strain of Toxoplasma gondii. J Parasitol 81:1032-1034, 1995.
Suzuki Y, Wong SW, Grumet FC, Fessel J, Montoya JG, Zolopa AR, Portimore A, Schmacher-Perdreau F, Schrappe M, Koppen S, Ruf B, Brown BW and Remington JS. Evidence for genetic regulation of susceptibility to toxoplasmic encephalitis in AIDS patients. J Infect Dis 173:265-268, 1996.
Suzuki Y, Yang Q, Yang S, Nguyen N, Lim, S, Liesenfeld O, Kojima T and Remington JS. IL-4 is protective against development of toxoplasmic encephalitis. J Immunol 157:2564-2569, 1996.
Liesenfeld O, Kosek J, Remington JS and Suzuki Y. Association of CD4+ T cell-dependent, IFN-g-mediated necrosis of the small intestine with genetic susceptibility to mice to peroral infection with Toxoplasma gondii. J Exp Med 184:597-607, 1996.
Suzuki Y, Rani S, Liesenfeld O, Kojima T, Lim S, Nguyen TA, Darlymple SA, Murray R and Remington JS. Impaired resistance to the development of toxoplasmic encephalitis in interleukin-6-deficient mice. Infect Immun 65:2339-2345, 1997.
Liesenfeld O, Kosek J and Suzuki Y. Interferon induces Fas-dependent apoptosis of peyer's patch T cells in mice following peroral infection with Toxoplasma gondii. Infect Immun 65:4682-4689, 1997.
Neyer LE, Kang H, Remington JS and Suzuki Y. Mesenteric lymph node T cells but not splenic T cells maintain their proliferative response to Concanavalin A following peroral infection with Toxoplasma gondii. Parasite Immunol. 20:573-581, 1998.
Liesenfeld O, Nguyen TA, Parkhe CV, Kang H, Watanabe H, Abo T, Sher A, Remington JS and Suzuki Y. TNF-a, nitric oxide and IFN-g are all critical for development of necrosis in the small intestine of genetically susceptible mice infected perorally with Toxoplasma gondii. Parasite Immunol. 22:365-376, 1999.
Suzuki Y. Genes, cells and cytokines in resistance against development of toxoplasmic encephalitis. Immunboil. 201:255-271, 1999.
Kang H, Remington JS and Suzuki Y. Decreased resistance of B cell-deficient mice to infection with Toxoplasma gondii despite unimpaired expression of IFN-g, TNF-a and inducible nitric oxide synthase. J. Immunol. 164:2629-2634, 2000.
Suzuki Y, Kang H, Parmley S and Park D. Induction of TNF-a and inducible nitric oxide synthase fails to prevent toxoplasmic encephalitis in the absence of IFN-g in genetically resistant BALB/c mice. Microbes Infect. 2:455-462, 2000.
Kang, H. and Suzuki, Y. Requirement of non-T cells that produce interferon-gamma for prevention of reactivation of Toxoplasma gondii infection in the brain. Infect. Immun. 69:2920-2927, 2001.
Grigg, ME, Bonnefoy, S., Hehl, A. B., and Suzuki, Y*, Boothroyd, J. C*. Success and virulence in Toxoplasma as the results of sexual recombination between two distinct ancectries. Science 294:161-165, 2001. *joint corresponding authors.
Suzuki, Y. Immunopathogenesis of cerebral toxoplasmosis. J Infect Dis 186:S236-240, 2002.
Kang, H., Liesendfeld, O., Remington, J. S., Claflin J., Wang, X., and Suzuki, Y. TCR Vb8+ T cells prevent development of toxoplasmic encephalitis in BALB/c mice genetically resistant to the disease. J. Immunol. 170:4254-4259, 2003.
Wang, X., Kang, H., Kikuchi, T., and Suzuki, Y. Gamma interferon production, but not perforin-mediated cytolytic activity, of T cells is required for prevention of toxoplasmic encephalitis in BALB/c mice genetically resistant to the disease. Infect. Immun. 72:4432-4438, 2004.