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Christopher J. Atkins

Researcher at National Institute for Medical Research

Publications -  10
Citations -  4597

Christopher J. Atkins is an academic researcher from National Institute for Medical Research. The author has contributed to research in topics: CD40 & Interleukin 21. The author has an hindex of 8, co-authored 10 publications receiving 4376 citations.

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TGFβ in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-Producing T cells

TL;DR: The data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation ofIL-17-producing T cells.
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Neuron and glia generating progenitors of the mammalian enteric nervous system isolated from foetal and postnatal gut cultures

TL;DR: The findings establish the feasibility of expanding and isolating early progenitors of the enteric nervous system based on their ability to form distinct neurogenic and gliogenic structures in culture and provide the rationale for the development of novel approaches to the treatment of congenital megacolon based on the colonisation of the aganglionic gut with progenitor derived from normoganglionics bowel segments.
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CD25+ CD4+ T cells compete with naive CD4+ T cells for IL-2 and exploit it for the induction of IL-10 production.

TL;DR: O adoptive transfer into lymphopenic mice showed that CD25+ CD4+ T cells interfere with CD25 up-regulation on co-transferred naive T cells, while increasing their own CD25 levels, providing a link explaining the apparent difference in regulatory mechanisms in vitro and in vivo.
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Multipotential progenitors of the mammalian enteric nervous system capable of colonising aganglionic bowel in organ culture.

TL;DR: The data show the NC-derived RET+ population of fetal gut in mammalian embryos consists of multipotential progenitors capable of colonising efficiently both wild-type and RET-deficient aganglionic bowel in organ culture.
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Modulation of Dendritic Cell Function by Naive and Regulatory CD4+ T Cells

TL;DR: Mutual interactions between DC and CD4+ T cell subpopulations following contact with pathogens are likely to influence the strength and quality of incipient immune responses in the local microenvironment.