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1 ptide-specific lysis by neighboring T cells (fratricide).
2 e of residual CD7 expression and the ensuing fratricide.
3 l and malignant cells, leading to CAR T-cell fratricide.
4 he pancreas, resulting in Fas/Fas-L-mediated fratricide.
5 between CARTs and T-ALL blasts leads to CART fratricide.
6 ded protection from CD70 CAR T cell-mediated fratricide.
7 d bacteriocins A and B (CibAB) implicated in fratricide.
10 age increase in load that is attributable to fratricide and determine the parameters that should be m
11 ic disruption of the CD7 gene prevented this fratricide and enabled expansion of CD7 CAR T cells with
13 CAR) T-cells targeting CCR9 are resistant to fratricide and have potent antileukemic activity both in
14 ve cytotoxicity and proliferation because of fratricide and not due to the absence of a 2B4-dependent
15 and some myeloid leukemias, produces robust fratricide and often requires additional mitigation stra
17 Additionally, we address the phenomenon of fratricide and trogocytosis-associated exhaustion, which
19 ade lymphodepleting serotherapy, CAR7 T-cell fratricide, and graft-versus-host disease, respectively.
22 es additional gene modifications to overcome fratricide because of shared T-cell antigens on normal a
24 ped a CD5-directed CAR that produces minimal fratricide by downmodulating CD5 protein levels in trans
31 ve HTLV-I-positive patients considered here, fratricide has probably caused an increase in equilibriu
32 tion and are susceptible to NK cell-mediated fratricide in a perforin- and NKG2D-dependent manner.
36 multiple turnovers, resulting in "molecular fratricide." N-bromoacetyltryptamine should serve as a u
37 ntigens may be limited by T cell aplasia and fratricide, necessitating "rescue" allogeneic hematopoie
38 of stationary phase cells mimics aspects of fratricide observed in enterococcal biofilms, where both
39 ets (RIP-Fas-L) as a result of Fas-dependent fratricide of beta-cells after transfer of diabetogenic
40 mic disruption of a target antigen overcomes fratricide of CAR T cells and establishes the feasibilit
41 nd malignant T cells, potentially leading to fratricide of CAR T cells or profound immunodeficiency.
43 pping expression on healthy T cells leads to fratricide of CD7-CAR T cells, requiring additional gene
44 m APCs in an Ag-specific fashion, leading to fratricide of programmed death 1-expressing, neighboring
45 T cells and show that they induce selective fratricide of SLAMF7(+/high) NK cells, CD4(+) and CD8(+)
46 lls, failed to trigger a self-MHC-restricted fratricide of T cells, and was associated with toxicity
47 inuous CAR-mediated engagement, resulting in fratricide of trogocytic antigen-expressing NK cells (NK
50 de-based CAR, which show evidence of minimal fratricide post activation/transduction and antigen-depe
55 data support the therapeutic and safe use of fratricide-resistant CD1a-CARTs for relapsed/refractory
56 ukemia (T-ALL) by self-selecting for CD7(-), fratricide-resistant CD7 CAR T cells that were transcrip
57 WU-CART-007 is a CD7-targeting, allogeneic, fratricide-resistant chimeric antigen receptor T-cell pr
58 dings demonstrate the efficacy and safety of fratricide-resistant, allogeneic anti-CD70 CAR T cells t
59 ls were completely resistant to DARA-induced fratricide, showed superior persistence in immune-defici
61 atibility complexes and became the target of fratricide T cell killing, which was reversed by Tim-3 b
62 ver-infiltrating cells, pointing to death by fratricide that causes almost complete disappearance of
63 on of competence for transformation, such as fratricide, the kin-discriminatory killing of neighborin
65 system prevented trogocytic antigen-mediated fratricide, while sparing activating CAR signaling again
66 athematical techniques to investigate T-cell fratricide with particular reference to HTLV-I infection