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Aymen Al-Shamkhani

Researcher at University of Southampton

Publications -  88
Citations -  5105

Aymen Al-Shamkhani is an academic researcher from University of Southampton. The author has contributed to research in topics: Cytotoxic T cell & CD8. The author has an hindex of 38, co-authored 83 publications receiving 4486 citations. Previous affiliations of Aymen Al-Shamkhani include University of Cambridge & University of Oxford.

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Viral infection switches non-plasmacytoid dendritic cells into high interferon producers

TL;DR: The results suggest that multiple dendritic cell types, not just plasmacytoid cells, can act as specialized interferon-producing cells in certain viral infections, and reveal the existence of a TLR-independent pathway for d endritic cell activation that can be the target of viral interference.
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Interaction with FcγRIIB Is Critical for the Agonistic Activity of Anti-CD40 Monoclonal Antibody

TL;DR: An essential cross-linking role for the inhibitory FcγRIIB in anti-CD40 immunostimulatory activity is demonstrated and it is suggested that isotype will be an important issue when optimizing reagents for clinical use.
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CD134L expression on dendritic cells in the mesenteric lymph nodes drives colitis in T cell-restored SCID mice.

TL;DR: Results indicate that some DC in the MLNs of SCID mice express an activated phenotype and that CD134L expression by these cells is involved in the development of colitis induced by T cell transfer, suggesting that inhibition of the accumulation of activated DC is one mechanism by which these cells prevent immune pathology.
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Combination CTLA-4 Blockade and 4-1BB Activation Enhances Tumor Rejection by Increasing T-Cell Infiltration, Proliferation, and Cytokine Production

TL;DR: This study shows that combining T-cell co-inhibitory blockade with αCTLA-4 and active co-stimulation with α4-1BB promotes rejection of B16 melanoma in the context of a suitable vaccine.
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Expression and costimulatory effects of the TNF receptor superfamily members CD134 (OX40) and CD137 (4-1BB), and their role in the generation of anti-tumor immune responses.

TL;DR: stimulation of CD137 in vivo is considerably more effective than CD134 in augmenting anti‐tumor immune responses, and agents that stimulate signaling via CD137 are likely to be more useful in clinical conditions where highly effective CD8+ CTL responses are required.