Sentences with phrase «t cell viability»

Not exact matches

Unlike for ccr5, there are no known humans with loss of function cxcr4 mutations that would provide insight into the safety and viability of cxcr4 disruption in mature CD4 + T cells.

Thus, treatment with X4 - ZFNs of both wild - type and ccr5Δ32 CD4 + T cells confers stable cxcr4 disruption and a marked survival advantage in the presence of R5X4 - HIV and X4 - HIV in vitro without any detectable effect on cell growth or viability in the absence of HIV.

For (D)--(F), 5 × 104 Stemcell Technologies — purified naive CD8 + T cells were incubated with 0.3 μg / ml anti-CD3 Ab at 37 °C for 72 h. Cells were surface - stained for viability and evaluated for proliferation as assessed by dilution of CFSE within CD8 + - gated cellscells were incubated with 0.3 μg / ml anti-CD3 Ab at 37 °C for 72 h. Cells were surface - stained for viability and evaluated for proliferation as assessed by dilution of CFSE within CD8 + - gated cellsCells were surface - stained for viability and evaluated for proliferation as assessed by dilution of CFSE within CD8 + - gated cellscells (D).

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.