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Mark A. A. Claassen

Researcher at Erasmus University Rotterdam

Publications -  31
Citations -  776

Mark A. A. Claassen is an academic researcher from Erasmus University Rotterdam. The author has contributed to research in topics: Hepatitis C & Hepatitis C virus. The author has an hindex of 15, co-authored 27 publications receiving 643 citations.

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Abundant numbers of regulatory T cells localize to the liver of chronic hepatitis C infected patients and limit the extent of fibrosis.

TL;DR: It is demonstrated that large numbers of highly activated and differentiated CD4+FoxP3+ Treg localize to the infiltrated chronic HCV-infected liver and may result in limiting the extent of fibrosis, suggesting that CD4 + FoxP3 + Treg play a pivotal role in limiting collateral damage by suppressing excessiveHCV-induced immune activation.
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Intrahepatic regulatory T cells are phenotypically distinct from their peripheral counterparts in chronic HBV patients

TL;DR: The data suggest that the higher proportion of intrahepatic Treg observed in patients with a high viral load may explain the lack of control of viral replication, and are phenotypically distinct from peripheral blood Treg.
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Frequencies of Circulating MAIT Cells Are Diminished in Chronic HCV, HIV and HCV/HIV Co-Infection and Do Not Recover during Therapy.

TL;DR: It is shown that the frequencies of MAIT cells are reduced in blood of patients with CHCV, HIV and in AHCV/HIV co-infection compared to healthy individuals, and the impact of HIV and HCV infection on the numbers and function ofMAIT cells warrant further studies on the effect of viral infections and the antimicrobial function.
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Retention of CD4+ CD25+ FoxP3+ Regulatory T Cells in the Liver after Therapy-Induced Hepatitis C Virus Eradication in Humans

TL;DR: It is indicated that successful antiviral therapy of chronic HCV patients does not lead to normalization of the local immune response to a resting state comparable to that for healthy livers, and the continuous presence of high numbers of Treg suggests ongoing residual regulation of immunopathology.