Abstract |
Inhibition of T cell function is an important pathological feature in malaria. We investigated which T cell population is reduced contributing to immunosuppression. We examined protein and RNA level of various cell receptors, specific for T cells in children having Plasmodium falciparum infection and compared those to healthy children of the same age. We observe reduced levels of cluster of differentiation (CD)3 and T cell receptor (TCR)alphabeta in both RNA and protein expression level. This reduced expression was associated with a collapsed membrane asymmetry as determined by enhanced annexinV binding. Also human leukocyte antigen ( HLA)-A,B,C- and HLA-DR-positive cells increasingly bound annexinV. The enhanced binding of annexinV was paralleled by a reduced expression of transcription factors such as T cell transcription factor 7 and GATA binding protein 3, which are involved in the expression of T cell specific genes. Also the expression of the transcription factors major histocompatibility complex class II transactivator and regulatory factor X 5, which are part of the HLA transcription machinery, is reduced during infection. We show that two mechanisms may lead to a suppression of the immune system during malaria: cell damage and reduction of gene expression of the CD3/TCR complex.
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Authors | Yvonne Kalmbach, Angelica B W Boldt, Benjamin Mordmüller, Maryvonne Kombila, Martin P Grobusch, Peter G Kremsner, Jürgen F J Kun |
Journal | Parasitology research
(Parasitol Res)
Vol. 104
Issue 3
Pg. 575-82
(Feb 2009)
ISSN: 0932-0113 [Print] Germany |
PMID | 18975003
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Annexin A5
- CD3 Complex
- Receptors, Antigen, T-Cell, alpha-beta
- Transcription Factors
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Topics |
- Animals
- Annexin A5
(metabolism)
- CD3 Complex
(biosynthesis)
- Cell Membrane
(metabolism)
- Child
- Child, Preschool
- Humans
- Immunosuppression Therapy
- Infant
- Malaria, Falciparum
(immunology)
- Plasmodium falciparum
(immunology)
- Receptors, Antigen, T-Cell, alpha-beta
(biosynthesis)
- Transcription Factors
(biosynthesis)
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