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Christophe Ferrand

Researcher at French Institute of Health and Medical Research

Publications -  148
Citations -  4653

Christophe Ferrand is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Transplantation & Cytotoxic T cell. The author has an hindex of 34, co-authored 142 publications receiving 4114 citations. Previous affiliations of Christophe Ferrand include Imperial College London & Netherlands Cancer Institute.

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Administration of herpes simplex–thymidine kinase–expressing donor T cells with a T-cell–depleted allogeneic marrow graft

TL;DR: Overall, the administration of low numbers of HS-tk-expressing T cells early following an HLA-identical BMT is associated with no acute toxicity, persistent circulation of the GMCs, and GCV-sensitive GVHD, and open the way to the infusion of higher numbers of gene-modified donor T cells to enhance post-BMT immune competence while preserving GCv-sensitive alloreactivity.
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Evidence of premature immune aging in patients thymectomized during early childhood

TL;DR: It is shown that young adults thymectomized during early childhood exhibit an altered T cell compartment and this condition was directly related to CMV infection and the induction of strong CMV-specific T cell responses, which may exhaust the naive T cell pool in the absence of adequate T cell renewal from the thymus.
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Relevance of Toll-like receptor-4 polymorphisms in renal transplantation.

TL;DR: RTR with TLR4 polymorphism present a lower risk of post-transplant atherosclerotic events and acute allograft rejection, but experience severe infectious episodes more frequently.
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Extended diagnostic criteria for plasmacytoid dendritic cell leukaemia.

TL;DR: This study validated pDCL‐specific markers for diagnosis by flow‐cytometry or quantitative reverse transcription polymerase chain reaction on bone marrow samples and proposed a diagnosis strategy, scoring first the CD4+ CD56+/− MPOneg cCD3neg cCD79aneg CD11cneg profile and then the CD123high,BDCA‐2 and BDCA‐4 expression.