J
J. Paul Mitchell
Researcher at Cardiff University
Publications - 5
Citations - 1431
J. Paul Mitchell is an academic researcher from Cardiff University. The author has contributed to research in topics: Exosome & Interleukin 21. The author has an hindex of 5, co-authored 5 publications receiving 1287 citations.
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Journal ArticleDOI
Human Tumor-Derived Exosomes Selectively Impair Lymphocyte Responses to Interleukin-2
TL;DR: The data show an exosome-mediated mechanism of skewing IL-2 responsiveness in favor of regulatory T cells and away from cytotoxic cells, which strongly implicates the role of exosomes in tumor immune evasion.
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Human Tumor-Derived Exosomes Down-Modulate NKG2D Expression
Aled Clayton,J. Paul Mitchell,Jacquelyn Court,S.J. Linnane,Malcolm David Mason,Zsuzsanna Tabi +5 more
TL;DR: The data show that NKG2D is a likely physiological target for exosome-mediated immune evasion in cancer, and lymphocyte effector function was impaired by pretreatment with tumor exosomes, as these cells exhibited poor NKG 2D-dependent production of IFN-γ and poor NKg2D- dependent killing function.
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Can urinary exosomes act as treatment response markers in prostate cancer
J. Paul Mitchell,Joanne L. Welton,John Staffurth,Jacquelyn Court,Malcolm David Mason,Zsuzsanna Tabi,Aled Clayton +6 more
TL;DR: Evaluating urinary-exosomes remains difficult, given the variability of exosomes in urine specimens, but this approach holds promise as a non-invasive source of multiple markers of malignancy that could provide clinically useful information.
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Increased exosome production from tumour cell cultures using the Integra CELLine Culture System.
TL;DR: The Integra CELLine culture system is used to achieve a significant increase in obtainable exosomes from adherent and non-adherent tumour cells, and should prove advantageous in future studies of exosome-immune modulation in cancer and other settings.
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TGFβ Induces a SAMHD1-Independent Post-Entry Restriction to HIV-1 Infection of Human Epithelial Langerhans Cells
Magdalena A. Czubala,Katja Finsterbusch,Matthew Owen Ivory,J. Paul Mitchell,Zahra Ahmed,Takatoshi Shimauchi,Richard O. S. Karoo,Sion Coulman,C. Gateley,James Caradoc Birchall,Fabien Blanchet,Vincent Piguet +11 more
TL;DR: It is demonstrated that transforming growth factor-β signaling confers this potent HIV-1 restriction in MDLC during their differentiation and blocking of mothers against decapentaplegic homolog 2 (SMAD2) signaling inMDLC restores cells' infectivity, which may explain why HIV- 1 acquisition is increased during coinfection with sexually transmitted infections.