Modulation of innate immunity by African Trypanosomes

The experimental studies of Brucei group trypanosomes presented here demonstrate that the balance of host and parasite factors, especially IFN-γ GPI-sVSG respectively, and the timing of cellular exposure to them, dictate the predominant MP and DC activation profiles present at any given time during...

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Bibliographic Details
Published inParasitology Vol. 137; no. 14; pp. 2051 - 2063
Main Authors PAULNOCK, DONNA M., FREEMAN, BAILEY E., MANSFIELD, JOHN M.
Format Journal Article
LanguageEnglish
Published Cambridge, UK Cambridge University Press 01.12.2010
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Summary:The experimental studies of Brucei group trypanosomes presented here demonstrate that the balance of host and parasite factors, especially IFN-γ GPI-sVSG respectively, and the timing of cellular exposure to them, dictate the predominant MP and DC activation profiles present at any given time during infection and within specific tissues. The timing of changes in innate immune cell functions following infection consistently support the conclusion that the key events controlling host resistance occur within a short time following initial exposure to the parasite GPI substituents. Once the changes in MP and DC activities are initiated, there appears little that the host can do to reverse these changes and alter the final outcome of these regulatory events. Instead, despite the availability of multiple innate and adaptive immune mechanisms that can control parasites, there is an inability to control trypanosome numbers sufficiently to prevent the emergence and establishment of virulent trypanosomes that eventually kill the host. Overall it appears that trypanosomes have carefully orchestrated the host innate and adaptive immune response so that parasite survival and transmission, and alterations of host immunity, are to its ultimate benefit.
Bibliography:ark:/67375/6GQ-0VWM2NLX-C
ArticleID:00146
istex:F3BD6917F1102F7131F9144BEA95C558171EB2EB
PII:S0031182010001460
ObjectType-Article-2
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ObjectType-Feature-3
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ISSN:0031-1820
1469-8161
DOI:10.1017/S0031182010001460