Sentences with phrase «t cell apoptosis»

Since the cancer cells in both types of tumors were the same, the researchers compared the noncancerous cells present in the induced and transplanted tumors to explore what might be causing the T cell apoptosis.

Not exact matches

Their paper, which appears in Nature Communications, describes how an immune cell recruited to the tumor induces the programmed suicide, or apoptosis, of the killer T cells harnessed by many immunotherapies.

Not only do controllers have more CD8 T cells, each cell produces greater quantities of perforin and granzymes, which stimulate apoptosis, or cell death.

By contrast, DN T cells are able to mediate DTH to donor alloantigens and induce apoptosis of donor - specific corneal endothelial cells.

The present demonstration of T cell - mediated apoptosis of allogeneic corneal cells from CD4 KO mice is consistent with previous findings, which noted the presence of apoptotic keratocytes and corneal endothelial cells in rejected corneal allografts in humans and rats respectively (5, 32).

In our study, CD8 − T cells from CD4 KO rejector mice failed to display CTL or DTH activity, yet they were capable of inducing donor - specific apoptosis of corneal endothelial cells.

Rejection by CD8 + T cells does not appear to involve either allospecific CTL or DTH effector mechanisms; however, CD8 + T cells are able to induce significant apoptosis of allogeneic corneal endothelial cells.

The role of DN T cells in corneal allograft rejection was confirmed in two separate in vitro assays in which CD8 − cells were isolated from CD4 KO donors that had rejected corneal allografts and were found to induce apoptosis of donor - specific corneal cells.

The results indicated that CD8 − T cells induced significant, albeit weak, apoptosis of allogeneic corneal epithelial cells (Figure 5A).

The extensive apoptosis of allogeneic corneal endothelial cells by CD8 − T cells from CD4 KO mice was perplexing, as this cell population should not contain CD4 + cells.

However, lymphocytes isolated from recipients of either CD8 + T cells or CD8 − T cells produced significant in vitro apoptosis of donor - specific corneal endothelial cells.

Additional studies are attempting to determine if the transgene expression of various anti-apoptotic genes can protect T cells from tumor - induced apoptosis.

Apoptosis has been implicated as a T cell - dependent immune effector mechanism in various forms of organ graft rejection (29 — 31).

The synthetic peptide PFWT disrupts AF4 — AF9 protein complexes and induces apoptosis in t (4; 11) leukemia cells.

Effect of presenilins in the apoptosis of thymocytes and homeostasis of CD8 + T cells.

Moreover, there are yet other cell types — such as visceral adipose tissue macrophages and cytotoxic CD8 + T - cells — in which the age - related supernumerary accumulation of dysfunctional and apoptosis - resistant cells appears to play a highly deleterious role on tissue function, but where the cells are not «senescent» cells in the classical sense of p16Ink4a expression and the senescence - associated secretory profile observed in senescent fibroblasts.

Binding of PD - L1 to the co-stimulatory receptor on T cells, PD - 1, promotes inactivation and apoptosis of activated anti-tumor T cells.

Tumor - associated B7 - H1 promotes T - cell apoptosis: a potential mechanism of immune evasion.

These include T - cell depletion by apoptosis; anergy (ie, the process by which T cells that are presented with a peptide in the absence of costimulatory signals become refractory to further stimulation with the antigen and are therefore inactivated); and the development of regulatory T cells, which can actively suppress antigen - specific responses following re-challenge with the antigen.

Manipulating the bioenergetics of alloreactive T cells causes their selective apoptosis and arrests graft - versus - host disease.

It was shown that VPA could induce the apoptosis of activated T cells and maintain immune homeostasis through the caspase - 8 / caspase - 3 pathway (28).

In a xenograft KMT2D - mutated T - lymphoma model, dual treatment with chidamide and decitabine significantly retarded tumor growth and induced cell apoptosis through modulation of the KMT2D / H3K4me axis.

Thus, VPA did not reduce GVHD by inducing apoptosis of CD4 + effector T cells.

This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.

We then examined whether VPA regulated immune homeostasis and ameliorated GVHD through inducing apoptosis of CD4 + T cells in vivo.

Approximately 50 % of PTCL are unclassifiable and categorized as PTCL, not otherwise specified (PTCL - NOS).1 Using gene expression profiling, PTCL - NOS lymphocytes can be distinguished from normal T lymphocytes, with deregulation of genes involved in apoptosis, proliferation, cell adhesion, and transcription regulation.2 Two subgroups of PTCL - NOS have been identified, which are characterized by high expression of either GATA3 or TBX21 / T - bet transcription factors and downstream target genes.3 However, actionable biomarkers closely related to the pathogenic mechanism need to be further investigated and may become potential therapeutic targets of PTCL - NOS. 4, 5

Cultures of senescent CD8 (+) T cells also show resistance to apoptosis, permanent loss of CD28 expression, altered cytokine profiles, reduced ability to respond to stress, and various functional changes.

Manfe V, Biskup E, Rosbjerg A, Kamstrup M, Skov AG, Lerche CM, Lauenborg BT, Odum N and Gniadecki R. miR - 122 regulates p53 / Akt signalling and the chemotherapy - induced apoptosis in cutaneous T - cell lymphoma.

Duntas (2015) articulates, «In susceptible individuals, iodine excess increases intra-thyroid infiltrating Th17 cells and inhibits T regulatory (Treg) cells development, while it triggers an abnormal expression of tumor necrosis factor - related apoptosis - inducing ligand (TRAIL) in thyrocytes, thus inducing apoptosis and parenchymal destruction» (31, p. 721).