γδ T-Cell Function in Pathogenesis of Cerebral Malaria in Mice Infected with<i>Plasmodium berghei</i>ANKA
-
- D. M. Yañez
- <!--label omitted: 1-->Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin
-
- J. Batchelder
- <!--label omitted: 1-->Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin
-
- H. C. van der Heyde
- <!--label omitted: 1-->Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin
-
- D. D. Manning
- <!--label omitted: 1-->Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin
-
- W. P. Weidanz
- <!--label omitted: 1-->Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin
-
- S. H. E. Kaufmann
- editor
書誌事項
- 公開日
- 1999-01
- 権利情報
-
- https://journals.asm.org/non-commercial-tdm-license
- DOI
-
- 10.1128/iai.67.1.446-448.1999
- 公開者
- American Society for Microbiology
この論文をさがす
説明
<jats:title>ABSTRACT</jats:title><jats:p>Mice depleted of γδ T cells by monoclonal antibody treatment and infected with<jats:italic>Plasmodium berghei</jats:italic>ANKA did not develop cerebral malaria (CM). In striking contrast, δ<jats:sup>0/0</jats:sup>mice infected with<jats:italic>P. berghei</jats:italic>developed CM despite their γδ T-cell deficiency. γδ T cells appear to be essential for the pathogenesis of CM in mice having experienced normal ontogeny but not in mice genetically deprived of γδ T cells from the beginning of life.</jats:p>
収録刊行物
-
- Infection and Immunity
-
Infection and Immunity 67 (1), 446-448, 1999-01
American Society for Microbiology
