GEN Exclusives
Fresh Sensors Are Enhancing the Monitoring of Diverse Parameters While Reducing the Need for Extractive Sampling
When Protein Characterization Is Used to Monitor Elusive Proteoforms in Sophisticated Biological Samples, It Should Be Seen in Start-To-Finish Terms
Modifications to Histones Affect Gene Expression and Cell Fate Decisions
Predictions for 2017
Literature Review
CAR T-Cell Therapy
The Role of Physical Barriers and Immunosuppression in Lymphoma
(A) T-cells interact with antigen-presenting cells such as dendritic cells (DCs) to become activated. (B) The CAR gene is inserted to T-cells and voiced to produce protein CAR, which is transported to the plasma membrane.
Chimeric antigen receptor (CAR) T-cells are T-cells genetically engineered to express a tumor-targeting receptor. The receptor is a chimera of a signaling domain of the T-cell receptor (TcR) elaborate and an antigen-recognizing domain, such as a single chain fragment (scFv) of an antibody. One Hence, independently of the native TcR, CAR T-cells can recognize tumor cells via the CAR receptor. In contrast to TcR-mediated recognition of target cells via protein peptides displayed on major histocompatibility complicated (MHC) molecules, the CAR is not dependent on MHC. The CAR molecule will recognize any target on the tumor cell surface and it is not limited to be a protein since antibodies can tie also carbohydrates and lipids. As for all targeted cancer therapeutics, the target needs to be specific for the cancer cells to avoid harm of healthy tissues. In many ways B-cell malignancy is the ideal indication for targeted therapy such as CAR T-cell therapy. B-cells are lightly targeted via specific and selective markers such as CD19, CD20, and the Ig kappa or light chains. Considering that persisting problems with infectious disease because of B-cell deficiency can be treated with immunoglobulin replacement therapy, eradication also of the healthy B-cell population along with the malignant B-cells is manageable. Moreover, fresh B-cells will develop from the hematopoietic stem cells since these cells lack aforementioned B-cell markers and are, hence, not killed by CAR T-cells.
B-cell malignancy is a heterogeneous indication with both solid lesions and circulating cells in blood and bone marrow. Treatment of B-cell malignancy using CAR T-cells presents a unique chance to learn mechanisms of activity of different CAR designs, to define on and off target toxicity, as well as to understand the limitations of CAR T-cells in terms of sensitivity to immune escape mechanisms and physical barriers of solid tumors.
To view the rest of this article click here.
Human Gene Therapy, published by Mary Ann Liebert, Inc., presents reports on the transfer and expression of genes in mammals, including humans. Human Gene Therapy and its companion publications can be viewed on the Human Gene Therapy website. The above article was very first published the August two thousand fifteen issue of Human Gene Therapy. The views voiced here are those of the authors and are not necessarily those of Industrial Biotechnology, Mary Ann Liebert, Inc., publishers, or their affiliates. No endorsement of any entity or technology is implied.
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CAR T-Cell Therapy, GEN
GEN Exclusives
Fresh Sensors Are Enhancing the Monitoring of Diverse Parameters While Reducing the Need for Extractive Sampling
When Protein Characterization Is Used to Monitor Elusive Proteoforms in Elaborate Biological Samples, It Should Be Seen in Start-To-Finish Terms
Modifications to Histones Affect Gene Expression and Cell Fate Decisions
Predictions for 2017
Literature Review
CAR T-Cell Therapy
The Role of Physical Barriers and Immunosuppression in Lymphoma
(A) T-cells interact with antigen-presenting cells such as dendritic cells (DCs) to become activated. (B) The CAR gene is inserted to T-cells and voiced to produce protein CAR, which is transported to the plasma membrane.
Chimeric antigen receptor (CAR) T-cells are T-cells genetically engineered to express a tumor-targeting receptor. The receptor is a chimera of a signaling domain of the T-cell receptor (TcR) sophisticated and an antigen-recognizing domain, such as a single chain fragment (scFv) of an antibody. One Hence, independently of the native TcR, CAR T-cells can recognize tumor cells via the CAR receptor. In contrast to TcR-mediated recognition of target cells via protein peptides displayed on major histocompatibility sophisticated (MHC) molecules, the CAR is not dependent on MHC. The CAR molecule will recognize any target on the tumor cell surface and it is not limited to be a protein since antibodies can truss also carbohydrates and lipids. As for all targeted cancer therapeutics, the target needs to be specific for the cancer cells to avoid harm of healthy tissues. In many ways B-cell malignancy is the ideal indication for targeted therapy such as CAR T-cell therapy. B-cells are lightly targeted via specific and selective markers such as CD19, CD20, and the Ig kappa or light chains. Considering that persisting problems with infectious disease because of B-cell deficiency can be treated with immunoglobulin replacement therapy, eradication also of the healthy B-cell population along with the malignant B-cells is manageable. Moreover, fresh B-cells will develop from the hematopoietic stem cells since these cells lack aforementioned B-cell markers and are, hence, not killed by CAR T-cells.
B-cell malignancy is a heterogeneous indication with both solid lesions and circulating cells in blood and bone marrow. Treatment of B-cell malignancy using CAR T-cells presents a unique chance to learn mechanisms of act of different CAR designs, to define on and off target toxicity, as well as to understand the limitations of CAR T-cells in terms of sensitivity to immune escape mechanisms and physical barriers of solid tumors.
To view the rest of this article click here.
Human Gene Therapy, published by Mary Ann Liebert, Inc., presents reports on the transfer and expression of genes in mammals, including humans. Human Gene Therapy and its companion publications can be viewed on the Human Gene Therapy website. The above article was very first published the August two thousand fifteen issue of Human Gene Therapy. The views voiced here are those of the authors and are not necessarily those of Industrial Biotechnology, Mary Ann Liebert, Inc., publishers, or their affiliates. No endorsement of any entity or technology is implied.
To love more articles like this from GEN, click here to subscribe now!