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Bree Foley

Researcher at University of Western Australia

Publications -  37
Citations -  2716

Bree Foley is an academic researcher from University of Western Australia. The author has contributed to research in topics: Interleukin 21 & Transplantation. The author has an hindex of 15, co-authored 35 publications receiving 2294 citations. Previous affiliations of Bree Foley include Telethon Institute for Child Health Research & University of Minnesota.

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Cytomegalovirus infection drives adaptive epigenetic diversification of NK cells with altered signaling and effector function.

TL;DR: The emergence of diverse subsets of human NK cells selectively lacking expression of signaling proteins after human cytomegalovirus (HCMV) infection is described, uncovering a spectrum of epigenetically unique adaptive NK cell subsets that diversify in response to viral infection and have distinct functional capabilities compared to canonical NK cells.
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Cytomegalovirus reactivation after allogeneic transplantation promotes a lasting increase in educated NKG2C natural killer cells with potent function

TL;DR: The kinetics of the NK-cell response to CMV reactivation in human recipients after hematopoietic cell transplantation is characterized to support the emerging concept that CMV-induced innate memory-cell populations may contribute to malignant disease relapse protection and infectious disease control long after transplantation.
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NK cell CD16 surface expression and function is regulated by a disintegrin and metalloprotease-17 (ADAM17)

TL;DR: It is demonstrated that over-activation of ADAM17 in NK cells may be detrimental to their effector functions by down-regulating surface expression of CD16 and CD62L, and an important role for targeting ADam17 to prevent CD16 shedding and improve the efficacy of therapeutic antibodies is supported.
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Human Cytomegalovirus (CMV)-Induced Memory-like NKG2C+ NK Cells Are Transplantable and Expand In Vivo in Response to Recipient CMV Antigen

TL;DR: It is concluded that NKG2C+ memory-like NK cells are transplantable and require active or latent (subclinical) expression of CMV Ag in the recipient for clonal expansion of NK cells previously exposed to CMV in the donor.
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Targeting natural killer cells to acute myeloid leukemia in vitro with a CD16 x 33 bispecific killer cell engager and ADAM17 inhibition

TL;DR: In vitro studies highlight the potential of CD16 × 33 BiKE ± ADAM17 inhibition to enhance NK cell activation and specificity against CD33+ AML, which optimally could be applied in patients with relapsed AML or for adjuvant antileukemic therapy posttransplantation.