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2018 ; 8
(1
): 5549
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gab.com Text
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Genetic abrogation of immune checkpoints in antigen-specific cytotoxic
T-lymphocyte as a potential alternative to blockade immunotherapy
#MMPMID29615718
Zhang C
; Peng Y
; Hublitz P
; Zhang H
; Dong T
Sci Rep
2018[Apr]; 8
(1
): 5549
PMID29615718
show ga
T cell function can be compromised during chronic infections or through
continuous exposure to tumor antigens by the action of immune checkpoint
receptors, such as programmed cell death protein 1 (PD-1). Systemic
administration of blocking antibodies against the PD-1 pathway can restore T cell
function, and has been approved for the treatment of several malignancies,
although there is a risk of adverse immune-related side-effects. We have
developed a method for generating gene knockouts in human antigen (Ag)-specific
cytotoxic T-Lymphocyte (CTLs) using clustered regularly interspaced short
palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) genome editing.
Using this method, we generated several transduced CD4(+) or CD8(+)
antigen-specific polyclonal CTL lines and clones, and validated gene
modifications of the PD-1 gene. We compared these T-cell lines and clones with
control groups in the presence of programmed death-ligand 1 (PD-L1) and observed
improved effector functions in the PD1-disrupted cell group. Overall, we have
developed a versatile tool for functional genomics in human antigen-specific CTL
studies. Furthermore, we provide an alternative strategy for current cell-based
immunotherapy that will minimize the side effects caused by antibody blockade
therapy.
|*Gene Editing
[MESH]
|*Immunotherapy
[MESH]
|Antigens, Neoplasm/*immunology
[MESH]
|CRISPR-Cas Systems
[MESH]
|Humans
[MESH]
|Lymphocyte Activation
[MESH]
|Neoplasms/*drug therapy/immunology
[MESH]
|Programmed Cell Death 1 Receptor/*antagonists & inhibitors/genetics/immunology
[MESH]
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