Immune-factors regulating the development of experimental cerebral malaria in mice infected or coinfected with Plasmodium spp.

During malaria infection, innate responses are triggered to limit the maximum parasite density when it crosses certain threshold. Toll-like receptors signaling pathway, mononuclear phagocytes and NK cell-mediated cytotoxicity are known to have important roles in activation of protective innate immun...

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Main Author: Teo, Shun Xie.
Other Authors: School of Biological Sciences
Format: Final Year Project
Language:English
Published: 2011
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Online Access:http://hdl.handle.net/10356/45265
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Institution: Nanyang Technological University
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spelling sg-ntu-dr.10356-452652023-02-28T18:03:41Z Immune-factors regulating the development of experimental cerebral malaria in mice infected or coinfected with Plasmodium spp. Teo, Shun Xie. School of Biological Sciences A*STAR Singapore Immunology Network Laurent Renia Carla Claser DRNTU::Science::Biological sciences::Microbiology::Immunology During malaria infection, innate responses are triggered to limit the maximum parasite density when it crosses certain threshold. Toll-like receptors signaling pathway, mononuclear phagocytes and NK cell-mediated cytotoxicity are known to have important roles in activation of protective innate immunity to malaria. Therefore, we first assessed role in experimental cerebral malaria (ECM) pathogenesis of molecules (TRIF and IRF3) involved in innate immunity signal transduction. TRIF-deficient mice infected with PbAluc were susceptible to ECM and displayed increased parasite biomass, although peripheral parasitemia was comparable to WT mice. Conversely, mice infected with another parasite strain, PbA-BdS, did not develop ECM despite having similar parasitemia to WT group. IRF3-deficient mice infected with either PbAluc or PbA-BdS were ECM-resistant. Lastly, macrophages and NK cells role in suppression of PbA growth and ECM in mice coinfected with Plasmodium spp. was elucidated. Using transgenic mouse model, MaFIA, which allows conditional ablation of myeloid cells, we showed that depletion of these cells protected coinfected mice against ECM and decreased total parasitemia due to an effect on Py 17X 1.1 growth. However, it had no effect on PbA suppression. Similarly, conditional ablation of NK cells in NKDTR mice excluded involvement of NK cells in PbA suppression, although these mice did not develop ECM. Bachelor of Science in Biological Sciences 2011-06-10T06:17:28Z 2011-06-10T06:17:28Z 2011 2011 Final Year Project (FYP) http://hdl.handle.net/10356/45265 en Nanyang Technological University 36 p. application/pdf
institution Nanyang Technological University
building NTU Library
continent Asia
country Singapore
Singapore
content_provider NTU Library
collection DR-NTU
language English
topic DRNTU::Science::Biological sciences::Microbiology::Immunology
spellingShingle DRNTU::Science::Biological sciences::Microbiology::Immunology
Teo, Shun Xie.
Immune-factors regulating the development of experimental cerebral malaria in mice infected or coinfected with Plasmodium spp.
description During malaria infection, innate responses are triggered to limit the maximum parasite density when it crosses certain threshold. Toll-like receptors signaling pathway, mononuclear phagocytes and NK cell-mediated cytotoxicity are known to have important roles in activation of protective innate immunity to malaria. Therefore, we first assessed role in experimental cerebral malaria (ECM) pathogenesis of molecules (TRIF and IRF3) involved in innate immunity signal transduction. TRIF-deficient mice infected with PbAluc were susceptible to ECM and displayed increased parasite biomass, although peripheral parasitemia was comparable to WT mice. Conversely, mice infected with another parasite strain, PbA-BdS, did not develop ECM despite having similar parasitemia to WT group. IRF3-deficient mice infected with either PbAluc or PbA-BdS were ECM-resistant. Lastly, macrophages and NK cells role in suppression of PbA growth and ECM in mice coinfected with Plasmodium spp. was elucidated. Using transgenic mouse model, MaFIA, which allows conditional ablation of myeloid cells, we showed that depletion of these cells protected coinfected mice against ECM and decreased total parasitemia due to an effect on Py 17X 1.1 growth. However, it had no effect on PbA suppression. Similarly, conditional ablation of NK cells in NKDTR mice excluded involvement of NK cells in PbA suppression, although these mice did not develop ECM.
author2 School of Biological Sciences
author_facet School of Biological Sciences
Teo, Shun Xie.
format Final Year Project
author Teo, Shun Xie.
author_sort Teo, Shun Xie.
title Immune-factors regulating the development of experimental cerebral malaria in mice infected or coinfected with Plasmodium spp.
title_short Immune-factors regulating the development of experimental cerebral malaria in mice infected or coinfected with Plasmodium spp.
title_full Immune-factors regulating the development of experimental cerebral malaria in mice infected or coinfected with Plasmodium spp.
title_fullStr Immune-factors regulating the development of experimental cerebral malaria in mice infected or coinfected with Plasmodium spp.
title_full_unstemmed Immune-factors regulating the development of experimental cerebral malaria in mice infected or coinfected with Plasmodium spp.
title_sort immune-factors regulating the development of experimental cerebral malaria in mice infected or coinfected with plasmodium spp.
publishDate 2011
url http://hdl.handle.net/10356/45265
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