A new therapeutic potential for cancers: One CAR with 2 different engines

Tumor cells escape from immune recognition by several mechanisms such as down-regulating of MHC class I molecules, losing of tumor antigens, etc. The purpose of cancer immunotherapy is to robust or reconstruct the capacity of the immune system to recognize and kill tumor cells by overwhelming the me...

Full description

Saved in:
Bibliographic Details
Published in:Human vaccines & immunotherapeutics 2017-08, Vol.13 (8), p.1786-1788
Main Authors: Sheikhi, Abdolkarim, Jafarzadeh, Abdollah
Format: Article
Language:English
Subjects:
Antigens, Neoplasm - chemistry
Antigens, Neoplasm - immunology
Cell Line, Tumor
Humans
Immunotherapy, Adoptive - methods
Killer Cells, Natural - immunology
Letter
Lymphocyte Activation
Neoplasms - immunology
Neoplasms - therapy
Receptors, Antigen, T-Cell - genetics
Receptors, Antigen, T-Cell - immunology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Tumor cells escape from immune recognition by several mechanisms such as down-regulating of MHC class I molecules, losing of tumor antigens, etc. The purpose of cancer immunotherapy is to robust or reconstruct the capacity of the immune system to recognize and kill tumor cells by overwhelming the mechanisms by which tumors escape the immune response. One of the novel immunotherapeutic strategies were used to potentiate NK- and T cell functions is chimeric antigen receptor (CAR). CARs are composed of an antigen-binding domain of a molecule such as an antibody (that binds to a tumor associated antigens expressed on the surface of tumor cells) and an intracellular T cell activation domain. The CARs provide the recognition of target antigen in a MHC-independent manner. CAR-armed T cells may be unable to kill their targets in the absence of co-stimulators like NK cells. On the other hand, CAR-armed NK cells may also be unable to destroy their targets without receiving help signals from Th cells. Thus, if CAR-armed NK cells use together with CAR-armed T cells, NK cells will be aggregated to the tumor site. Thus, not only CAR T cells will obtain the necessary cytokines/costimulators from NK cells, but also other tumor specific T cells will be primed by recognition of tumor specific antigen (TSA) associated with MHC class I. These new specific primed T cells probably combat against tumor cells which have lost their TAAs that CAR-T cells are redirected to them.
ISSN:2164-5515
2164-554X
DOI:10.1080/21645515.2017.1314874