Brain immune cells characterization in UCMS exposed P2X7 knock-out mouse

2021 ◽  
Vol 94 ◽  
pp. 159-174
Author(s):  
Romain Troubat ◽  
Samuel Leman ◽  
Katleen Pinchaud ◽  
Alexandre Surget ◽  
Pascal Barone ◽  
...  
Keyword(s):  
Immune Cells ◽  
Knock Out ◽  
Knock Out Mouse

Histidine decarboxylase (HDC) knock out mouse immune cells have altered expression of ACTH, triiodothyronine and endorphin

2007 ◽  
Vol 56 (10) ◽  
pp. 428-431 ◽  
Author(s):  
G. Csaba ◽  
P. Kovács ◽  
E. Buzás ◽  
M. Mazán ◽  
É. Pállinger
Keyword(s):  
Immune Cells ◽  
Histidine Decarboxylase ◽  
Altered Expression ◽  
Knock Out ◽  
Knock Out Mouse

scholarly journals Mouse Mast Cell Protease-4-dependent production of ET-1 (1-31) and of plaque progression in an/INS; Apolipoprotein E knock-out mouse model of spontaneous atherosclerosis

Life Sciences ◽  
2013 ◽  
Vol 93 (25-26) ◽  
pp. e57
Author(s):  
Martin Houde ◽  
Walid Semaan ◽  
Louisane Desbiens ◽  
Zhipeng You ◽  
Adel G. Schwertani ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mouse Model ◽  
Apolipoprotein E ◽  
Plaque Progression ◽  
Knock Out ◽  
Mast Cell Protease ◽  
Mouse Mast Cell ◽  
Knock Out Mouse

scholarly journals A Potential Compensatory Role of Panx3 in the VNO of a Panx1 Knock Out Mouse Model

2018 ◽  
Vol 11 ◽  
Author(s):  
Paige Whyte-Fagundes ◽  
Stefan Kurtenbach ◽  
Christiane Zoidl ◽  
Valery I. Shestopalov ◽  
Peter L. Carlen ◽  
...  
Keyword(s):  
Mouse Model ◽  
Knock Out ◽  
Knock Out Mouse

Expression of globular form acetylcholinesterase is not altered in P2Y1R knock-out mouse brain

2016 ◽  
Vol 259 ◽  
pp. 291-294 ◽  
Author(s):  
Jane D. Cui ◽  
Miranda L. Xu ◽  
Etta Y.L. Liu ◽  
Tina T.X. Dong ◽  
H.Q. Lin ◽  
...  
Keyword(s):  
Mouse Brain ◽  
Knock Out ◽  
Globular Form ◽  
Knock Out Mouse

scholarly journals In Vitro Evaluation of CD276-CAR NK-92 Functionality, Migration and Invasion Potential in the Presence of Immune Inhibitory Factors of the Tumor Microenvironment

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1020
Author(s):  
Stefan Grote ◽  
Guillermo Ureña-Bailén ◽  
Kenneth Chun-Ho Chan ◽  
Caroline Baden ◽  
Markus Mezger ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Solid Tumors ◽  
Immune Cells ◽  
Immune Cell ◽  
Nk Cell ◽  
Migration And Invasion ◽  
Cellular Immunotherapy ◽  
Knock Out ◽  
Immunosuppressive Tumor Microenvironment

Background: Melanoma is the most lethal of all skin-related cancers with incidences continuously rising. Novel therapeutic approaches are urgently needed, especially for the treatment of metastasizing or therapy-resistant melanoma. CAR-modified immune cells have shown excellent results in treating hematological malignancies and might represent a new treatment strategy for refractory melanoma. However, solid tumors pose some obstacles for cellular immunotherapy, including the identification of tumor-specific target antigens, insufficient homing and infiltration of immune cells as well as immune cell dysfunction in the immunosuppressive tumor microenvironment (TME). Methods: In order to investigate whether CAR NK cell-based immunotherapy can overcome the obstacles posed by the TME in melanoma, we generated CAR NK-92 cells targeting CD276 (B7-H3) which is abundantly expressed in solid tumors, including melanoma, and tested their effectivity in vitro in the presence of low pH, hypoxia and other known factors of the TME influencing anti-tumor responses. Moreover, the CRISPR/Cas9-induced disruption of the inhibitory receptor NKG2A was assessed for its potential enhancement of NK-92-mediated anti-tumor activity. Results: CD276-CAR NK-92 cells induced specific cytolysis of melanoma cell lines while being able to overcome a variety of the immunosuppressive effects normally exerted by the TME. NKG2A knock-out did not further improve CAR NK-92 cell-mediated cytotoxicity. Conclusions: The strong cytotoxic effect of a CD276-specific CAR in combination with an “off-the-shelf” NK-92 cell line not being impaired by some of the most prominent negative factors of the TME make CD276-CAR NK-92 cells a promising cellular product for the treatment of melanoma and beyond.

CRISPR–Cas9 gene editing as a tool for developing immunotherapy for cancer

2021 ◽  
Author(s):  
Moataz Dowaidar
Keyword(s):  
T Cells ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Gene Editing ◽  
Genetically Engineered ◽  
Cancer Resistance ◽  
Knock Out ◽  
Tumor Tissues ◽  
Engineered T Cells ◽  
Long Time

T cells following genome editing and transformation might be detectable in peripheral blood and tumor tissues for a long time, even more than a year. The types and diversity of T-cells in peripheral blood and tumor tissues changed following transfusion of genetically modified T-cells, and some highly suspected T-cells targeting cancer cells grew, increasing the proportion of such cells. Moreover, after getting genetically engineered T cells, anticancer cytokine secretion increased. T cells changed by gene editing have certain functions, at least from an immunological standpoint. The first clinical research using the CRISPR–Cas9 gene editing method for cancer resistance is more complicated: Using CRISPR–Cas9 gene editing technology to concurrently knock out, amplify, activate and reinfuse three genes in human immune cells. This therapeutic strategy is more demanding, because the changed immune cells have a wider target scope. The data suggest that the efficacy of gene editing in immune cells was 15–45%, and the modified cells could survive long in the peripheral blood and tumor tissues of patients. After three or four months, some T-cells became central T-cells. These encouraging findings pave the way for future experimental cancer research utilizing CRISPR technology.

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