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Steven E. Macatonia

Researcher at Medical Research Council

Publications -  28
Citations -  8587

Steven E. Macatonia is an academic researcher from Medical Research Council. The author has contributed to research in topics: Dendritic cell & Antigen. The author has an hindex of 22, co-authored 28 publications receiving 8464 citations. Previous affiliations of Steven E. Macatonia include Washington University in St. Louis.

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Journal ArticleDOI

Development of TH1 CD4+ T cells through IL-12 produced by Listeria-induced macrophages

TL;DR: This regulatory pathway may have evolved to enable innate immune cells, through interactions with microbial pathogens, to direct development of specific immunity toward the appropriate TH1 phenotype.
Journal Article

Dendritic cells produce IL-12 and direct the development of Th1 cells from naive CD4+ T cells.

TL;DR: In addition to inducing proliferation and clonal expansion of naive T cells, dendritic cells, by their production of IL-12, play a direct role in the development of IFN-gamma-producing cells that are important for cell-mediated immune responses.
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Localization of antigen on lymph node dendritic cells after exposure to the contact sensitizer fluorescein isothiocyanate. Functional and morphological studies.

TL;DR: It is speculated that low amounts of FITC binding selectively to veiled cells or lymph node DC in the first hours after exposure to antigen are not immunogenic but that Langerhans' cells acquire high levels of antigen, enter the nodes, and initiate immune responses.
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T cell genetic background determines default t helper phenotype development in vitro

TL;DR: The results suggest that the genetically determined default Th phenotype development observed in vitro may correspond to in vivo Th subset responses for pathogens such as Leishmania which do not initiate strong Th phenotype-directing signals.
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B7 and interleukin 12 cooperate for proliferation and interferon gamma production by mouse T helper clones that are unresponsive to B7 costimulation.

TL;DR: It is shown that IL-12 can overcome the inhibitory effect of IL-10 for the APC-dependent induction of proliferation and IFN-gamma production by Th1 clones and may help to maintain these T cells in an unresponsive state during an inflammatory response.