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Hideyuki Nagasawa

Researcher at University of Tokushima

Publications -  27
Citations -  418

Hideyuki Nagasawa is an academic researcher from University of Tokushima. The author has contributed to research in topics: Heat shock protein & Toxoplasma gondii. The author has an hindex of 13, co-authored 27 publications receiving 415 citations. Previous affiliations of Hideyuki Nagasawa include Case Western Reserve University.

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Journal Article

Gamma delta T cells play an important role in hsp65 expression and in acquiring protective immune responses against infection with Toxoplasma gondii.

TL;DR: Findings indicated that gamma delta T cells having both the Thy-1+ and Thy- 1- phenotypes contribute to hsp65 expression within and on macrophages in an IFN-gamma-independent manner, which plays a role in the development of protective immunity during the early stage of this parasitic infection.
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Localization of circumsporozoite protein of Plasmodium ovale in midgut oocysts.

TL;DR: This work reports the first evidence that CS protein is present in oocyst sporozoites and sporoblasts of P. ovale oocysts, and indicates a uniform distribution of CS protein on these membranes.
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Induction of heat shock protein closely correlates with protection against Toxoplasma gondii infection.

TL;DR: HSP was demonstrable in mice that acquired resistance against infection with a lethal dose of bradyzoites of the Beverley strain or of an inoculum of a highly virulent strain of T. gondii.
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Plasmodium malariae: Distribution of circumsporozoite protein in midgut oocysts and salivary gland sporozoites

TL;DR: The distribution of the circumsporozoite protein within developing Plasmodium malariae oocysts and salivary gland sporozoites was examined by immunoelectron microscopy using protein A-gold and a monoclonal antibody specific for the CS protein of P. malariae.
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Role of L3T4+ and Lyt-2+ T cell subsets in protective immune responses of mice against infection with a low or high virulent strain of Toxoplasma gondii.

TL;DR: Lyt‐2+ T cells alone appear to be final effector cells for protection against the challenge with high virulent RH strain tachyzoites, since treatment of the bradyzoite‐immune mice with anti‐Lyt‐2 antibody, but not anti-L3T4 antibody, before challenge significantly increased mortality.