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Megan J. Barnden

Researcher at Alfred Hospital

Publications -  5
Citations -  2118

Megan J. Barnden is an academic researcher from Alfred Hospital. The author has contributed to research in topics: T cell & T-cell receptor. The author has an hindex of 5, co-authored 5 publications receiving 2000 citations.

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Defective TCR expression in transgenic mice constructed using cDNA-based alpha- and beta-chain genes under the control of heterologous regulatory elements

TL;DR: Results show that successful generation of MHC class II‐restricted, OVA‐specific αβTCR transgenic mice was dependent upon combining cDNA‐ and genomic DNA‐based constructs for expression of the respective α‐ and β‐chains of the TCR.
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CD4+ T Cell Help Impairs CD8+ T Cell Deletion Induced by Cross-presentation of Self-Antigens and Favors Autoimmunity

TL;DR: Data indicate that control of such help is critical for the maintenance of CD8+ T cell tolerance induced by cross-presentation, and indicates that provision of help favored induction of autoimmunity.
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Characterization of the ovalbumin-specific TCR transgenic line OT-I: MHC elements for positive and negative selection.

TL;DR: Results suggest that a lower affinity TCR:MHC interaction may be necessary for positive selection in FTOC compared with selection in situ, and the ability to select in vitro correlated with the capacity to present the ovalbumin (OVA) peptide to OT‐I cells, as measured by induction of an OVA‐specific proliferative response.
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Down-modulation of CD8 beta-chain in response to an altered peptide ligand enables developing thymocytes to escape negative selection.

TL;DR: A mechanism whereby developing thymocytes bearing an alphabetaTCR can modify their expression of the CD8 coreceptor to escape thymic deletion and achieve self-tolerance is suggested.
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Peptide antagonists that promote positive selection are inefficient at T cell activation and thymocyte deletion.

TL;DR: Both peripheral T cell activation and thymic deletion have an overall similar pattern of peptide specificity which differs from that required for positive selection, which suggests that a subset of major histocompatibility complex‐presented peptides could promote positive selection without causing either thymi deletion or peripheral activation of those selected T cells.