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J M Bridon

Researcher at Schering-Plough

Publications -  21
Citations -  3520

J M Bridon is an academic researcher from Schering-Plough. The author has contributed to research in topics: CD40 & B cell. The author has an hindex of 18, co-authored 21 publications receiving 3428 citations. Previous affiliations of J M Bridon include Netherlands Cancer Institute.

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Journal ArticleDOI

Selective Recruitment of Immature and Mature Dendritic Cells by Distinct Chemokines Expressed in Different Anatomic Sites

TL;DR: The observation that CCR6 mRNA expression decreases progressively as DCs mature, whereas CCR7 mRNA expression is sharply upregulated, provides a likely explanation for the changes in chemokine responsiveness, and suggests a role for MIP-3α/CCR6 in recruitment of immature DCs at site of injury and for Mip-3β/CCr7 in accumulation of antigen-loaded mature DCs in T cell–rich areas.
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Human Interleukin-10 Induces Naive Surface-immunoglobulin D+ (sigd(+)) B-cells To Secrete Igg1 and Igg3

TL;DR: It is reported that in response to interleukin 10 (IL-10), anti-CD40 activated tonsillar surface IgD+ (sIgD+) B cells are induced to secrete large amounts of IgM, IgG1, and IgG3 but neither IgG2 nor IgG4.
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Human dendritic cells skew isotype switching of cd40-activated naive b cells towards iga1 and iga2

TL;DR: Results suggest that in addition to activating T cells in the extrafollicular areas of secondary lymphoid organs, human D-Lc also directly modulate T cell–dependent B cell growth and differentiation, by inducing the IgA isotype switch.
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Subtractive hybridization reveals the expression of immunoglobulinlike transcript 7, Eph-B1, granzyme B, and 3 novel transcripts in human plasmacytoid dendritic cells

TL;DR: The identification of genes expressed in PDCs provides new insights into their function and origin and several novel molecules have been identified that were predicted to encode for a type 2 transmembrane protein (BRI(3), a putative cytokine (C-15, a cysteine-rich-secreted protein), and a type 1 leucine- rich repeat protein (MAPA).
Journal Article

The EBV IL-10 homologue is a selective agonist with impaired binding to the IL-10 receptor.

TL;DR: It is suggested that vIL-10 is a selective agonist that is impaired in its ability to bind the defined IL-10R, which is now designated as IL- 10R alpha.