Karlee Silver
University of Oxford
10 Papers
45 Citations
Karlee Silver is an academic researcher from University of Oxford. The author has contributed to research in topics: B cell & LYN. The author has an hindex of 7, co-authored 10 publications. Previous affiliations of Karlee Silver include Wellcome Trust Centre for Human Genetics & John Radcliffe Hospital.
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Papers
Enhancement and suppression of signaling by the conserved tail of IgG memory–type B cell antigen receptors
Keisuke Horikawa,Stephen Martin,Sarah L. Pogue,Karlee Silver,Kaiman Peng,Kiyoshi Takatsu,Christopher C. Goodnow +6 more
TL;DR: A novel “less-is-more” hypothesis is suggested to explain how switching to IgG enhances B cell memory responses, whereby decreased BCR signaling to genes that oppose marginal zone and plasma cell differentiation enhances the formation of these key cell types.
CD4 T cell-dependent autoimmunity against a melanocyte neoantigen induces spontaneous vitiligo and depends upon Fas-Fas ligand interactions.
Teresa Lambe,Janson C. H. Leung,Tiphaine Bouriez-Jones,Karlee Silver,Kimmo Makinen,Tanya L. Crockford,Helen Ferry,John V. Forrester,Richard J. Cornall +8 more
TL;DR: The findings show that CD4-dependent destruction of melanocytes is partially inhibited by blocking Fas-Fas ligand interactions and also highlights the importance of local control of autoimmunity, as vitiligo remains patchy and never proceeds to confluence even when Ag and autoreactive CD4+ T cells are abundant.
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Analysis of Lyn/CD22 double-deficient B cells in vivo demonstrates Lyn- and CD22-independent pathways affecting BCR regulation and B cell survival
Helen Ferry,Tanya L. Crockford,Karlee Silver,Nigel Rust,Christopher C. Goodnow,Richard J. Cornall +5 more
TL;DR: The results show that although the effects of Lyn are dominant in negative regulation of B cell hyperactivity, Lyn and CD22 have independent and additive effects on B cell survival, emphasize the subtle nature of regulation at the BCR and the usefulness of genetic complementation to dissect common and parallel pathways.
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Isotype control of B cell signaling.
Karlee Silver,Richard J. Cornall +1 more
TL;DR: Observations that stimulation through BCRs containing an IgG cytoplasmic tail causes increased numbers of antigen-specific clones to accumulate are a valuable step toward understanding the difference in B cell signaling between naïve and memory cells.
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TLR4, TLR9 and MyD88 are not required for the positive selection of autoreactive B cells into the primary repertoire.
TL;DR: The results suggest that the significant effects of TLR on autoimmunity occur in the established repertoire and not during B cell development, showing that TLR4, TLR9 and MyD88 are not required for the positive selection of autoreactive B cells in the primary B cell repertoire.
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