p53 - Based cyclotherapy: exploiting the «guardian of the genome» to protect normal cells
from cytotoxic therapy.
«Myeloid - derived suppressor cells (MDSCs) produce reactive nitrogen radicals that alter the receptors on the surface of the tumour to hide
it from cytotoxic lymphocytes that kill tumour cells.
Not exact matches
Histone deacetylase (HDAC) inhibitors have shown promise in «flushing out» HIV
from latently infected cells, potentially exposing the reservoirs available for elimination by
cytotoxic T lymphocytes (CTL), also called killer T cells.
The researchers also analyzed specific immune cells called
cytotoxic T cells isolated
from the patients» blood and found increases in biomarkers indicative of immune activation.
They are designed to get around one of the ways that cancer protects itself
from the immune system: tumors can activate the body's natural protective response
from autoimmunity, called a checkpoint, and thereby thwart
cytotoxic T cells.
In healthy skin, CD49a + and CD49a cells are dormant, but quickly respond with inflammatory and
cytotoxic effects when stimulated by IL - 15, a protein secreted
from skin cells as a rapid - response defence against microbial attack.
«We studied human T cells, isolated
from blood donors of all ages, to compare mature
cytotoxic T cells with naive ones,» said Philip Ansumana Hull, graduate student in Ott's lab and one of the first authors of the study.
First, new drugs could be developed to strengthen SIRT1 to rejuvenate mature
cytotoxic T cells or keep them
from progressing too quickly into a highly toxic state.
«We had some indication that rapamycin would enhance the
cytotoxic T cell effect,
from previous experiments in both animals and humans showing that the drug produced modest effects by itself,» says Maria Castro, Ph.D., senior author of the new paper.
Anichini A, Maccalli C, Mortarini R, Salvi S, Mazzocchi A, Squarcina P, Herlyn M, Parmiani G. Melanoma cells and normal melanocytes share antigens recognized by HLA - A2 - restricted
cytotoxic T cell clones
from melanoma patients.
New research
from La Jolla Institute for Allergy and Immunology lays the groundwork to parse how the virus interacts with its host and causes disease by pinpointing CD8 + T cells, a subset of T cells more commonly known as
cytotoxic or killer T cells, as important gatekeepers that control Zika infection or limit the severity of disease.
These agents will possibly increase the
cytotoxic action of MDR - related drugs by preventing the extrusion of anticancer drugs
from the target cells.
Our data suggests that targeting DGKζ could prove to be a more useful clinical approach to augment
cytotoxic T cell activity against tumor than targeting Cbl - b, perhaps resulting
from enhanced Ras / ERK signaling.
Thus apart
from direct
cytotoxic effect, the exposure of cancer cells to therapeutic doses of radiation also enhances the survival and proliferation of a fraction of cells which ultimately leads to radiation resistance and therapeutic inefficacy.
CD8 (+)
cytotoxic and CD4 (+) helper / inducer T cells develop
from common thymocyte precursors that express both CD4 and CD8 molecules.
This is associated with a relative reduction in
cytotoxic T - cell activity and a reduced capacity to destroy infected host cells and clear the virus
from infected lung tissue.
In cancer, Tregs are recruited by tumors and prevent other types of T cells, including
cytotoxic T cells (also called CD8 cells)
from attacking and destroying cancer cells.
Since amiodarone HCL is known to exert its
cytotoxic effect through the extrinsic, caspase - 9 independent apoptotic pathway [33] our microarray results confirm that the differential
cytotoxic effect seen in NSCs treated with amiodarone HCL is due to specific activation of extrinsic apoptosis pathways resulting
from exposure to the drug.
Importantly, this automated screening assay allowed us to interrogate some of the specific molecular mechanisms that may be responsible for the targeted
cytotoxic effect amiodarone HCL had on NSCs and not cells differentiated
from NSCs.