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Tomasz Ahrends

Researcher at Netherlands Cancer Institute

Publications -  17
Citations -  1760

Tomasz Ahrends is an academic researcher from Netherlands Cancer Institute. The author has contributed to research in topics: Cytotoxic T cell & CTL*. The author has an hindex of 10, co-authored 16 publications receiving 912 citations. Previous affiliations of Tomasz Ahrends include Gdańsk Medical University & Rockefeller University.

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CD4 + T cell help in cancer immunology and immunotherapy

TL;DR: This Review highlights the cellular dynamics and membrane receptors that mediate CD4+ T cell help and the molecular mechanisms of the enhanced antitumour activity of CTLs and discusses the molecular nature of help signals and how they can be harnessed to improve cancer immunotherapy.
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CD4+ T Cell Help Confers a Cytotoxic T Cell Effector Program Including Coinhibitory Receptor Downregulation and Increased Tissue Invasiveness

TL;DR: The gene expression signatures revealed that CD4+ T cell help during priming optimized CTLs in expression of cytotoxic effector molecules and many other functions that ensured efficacy of C TLs throughout their life cycle.
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Adrenergic Signaling in Muscularis Macrophages Limits Infection-Induced Neuronal Loss.

TL;DR: The results identify a mechanism of neuronal death post-infection and point to a role for tissue-resident MMs in limiting neuronal damage.
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CD27 Agonism Plus PD-1 Blockade Recapitulates CD4+ T-cell Help in Therapeutic Anticancer Vaccination

TL;DR: This work demonstrates in mice how CD4(+) T-cell help optimizes the CTL response to a clinically relevant DNA vaccine engineered to combat human papillomavirus-expressing tumors and provides a preclinical rationale to apply CD27 agonist antibodies, either alone or combined with PD-1 blockade, to improve the therapeutic efficacy of cancer vaccines and immunotherapy generally.
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CD4+ T cell help creates memory CD8+ T cells with innate and help-independent recall capacities

TL;DR: It is shown that during priming, CD4+ T cell help optimizes CTL memory by creating TEM cells with innate and help-independent antigen-specific recall capacities, as well as for innate-like recall responses by IL-12/IL-18 and promoting survival byIL-15.