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Michael J. Pinkoski

Researcher at La Jolla Institute for Allergy and Immunology

Publications -  34
Citations -  3627

Michael J. Pinkoski is an academic researcher from La Jolla Institute for Allergy and Immunology. The author has contributed to research in topics: Apoptosis & Fas ligand. The author has an hindex of 22, co-authored 34 publications receiving 3503 citations. Previous affiliations of Michael J. Pinkoski include University of Leicester & Children's Hospital of Eastern Ontario.

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Activation-induced cell death in T cells.

TL;DR: This review addresses the phenomenon of activation‐induced cell death (AICD) in T lymphocytes, in which activation through the T‐cell receptor results in apoptosis.
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CD4 + T-cell help controls CD8 + T-cell memory via TRAIL-mediated activation-induced cell death

TL;DR: Regulation of Trail expression can account for the role of CD4+ T cells in the generation of CD8+ T cell memory and represents a novel mechanism for controlling adaptive immune responses.
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Granzyme B short-circuits the need for caspase 8 activity during granule-mediated cytotoxic T-lymphocyte killing by directly cleaving Bid.

TL;DR: Granzyme B directly cleaves the proapoptotic molecule Bid, bypassing the need for caspase 8 activation of Bid, providing evidence for a two-pronged strategy for mediating target cell destruction and evidence of a direct link between granzyme B activity, Bid cleavage, and caspases 3 activation in whole cells.
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Granzyme B-mediated cytochrome c release is regulated by the Bcl-2 family members bid and Bax.

TL;DR: It is shown that cytochrome c release requires the direct proteolytic cleavage of Bid by grB to generate a 14-kD grB-truncated product (gtBid) that translocates to mitochondria and explains the caspase-independent mechanism of mitochondrial dysfunction.
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Entry and trafficking of granzyme B in target cells during granzyme B-perforin-mediated apoptosis.

TL;DR: A new model for granzyme-perforin-induced target cell lysis is proposed in which granzyme B is subjected to trafficking events in the target cell that control and contribute to cell death.