Sentences with phrase «+ t»

Together, these data indicate that peripheral T cell numbers are relatively preserved in KO or DKO mice compared with WT mice but that fewer naive CD8 + T cells are present in all genotypes when compared with WT.

Either way, this subset of CD4 + T cells could become a target for eradicating the virus.

The late - boost study, led by scientists from AFRIMS and the Thai Ministry of Health, found that vaccine boosts containing AIDSVAX B / E generated increased, but short - lived, humoral and CD4 + T - cell responses that did not rise further after subsequent boosting.

As an additional finding, we observed little stimulation of purified naive DGKζ - deficient CD8 + T cells, relative to Cbl - b — deficient or DKO cells (compare Fig. 3A with Fig. 3D), at limiting dilutions of anti-CD3 (0.3 μg / ml), when compared with DGKζ - deficient T cells in a mixed population.

Previous work with DGKζ − / − CD8 + T cells showed that increased TCR - mediated proliferation relative to WT T cells can be largely attributed to increased IL - 2 production (17, 25).

Collectively, these data indicate that DGKζ − / − mice exert improved control of orthotopically implanted KPC1242 tumors, compared with WT mice, in a manner that may result from changes in the number of intratumoral activated CD8 + T cells in DGKζ − / − mice.

Decreased diacylglycerol metabolism enhances ERK activation and augments CD8 + T cell functional responses.

The addition of IL - 2, as expected, enhanced the proliferation of WT T cells, but not completely to levels observed with DGKζ − / − CD8 + T cells + IL - 2 or to Cbl - b − / − and DKO CD8 + T cells (Fig. 3D).

Six weeks postinfection, splenocytes were analyzed for gp33 - LCMV — specific total CD8 + T cells (B) or short - lived effector cells and memory precursor effector cells (C).

A Marked Reduction in Priming of Cytotoxic CD8 + T Cells Mediated by Stress - Induced Glucocorticoids Involves Multiple Deficiencies in Cross-Presentation by Dendritic Cells.

ATF2 impairs glucocorticoid receptor — mediated transactivation in human CD8 + T cells.

As seen with stimulated T cells (Fig. 3C), Cbl - b − / − and DKO CD8 + T cells produced higher levels of IFN - γ compared with DGKζ − / − or WT CD8 + T cells (Fig. 3F) in a manner that was enhanced by the presence of additional IL - 2 (Fig. 3F).

Cutting edge: selective requirement for the Wiskott - Aldrich syndrome protein in cytokine, but not chemokine, secretion by CD4 + T cells.

A similar trend was observed in activated CD4 + T cells (Supplemental Fig. 1).

Although similar numbers of total splenic gp33 - LCMV — specific T cells were observed between genotypes (Fig. 5B), the distribution of gp33 - LCMV — specific CD8 + T cell effector and memory subsets were altered, such that there was a significantly lower percentage of short - term effector T cells and reciprocal changes in memory precursor cells among gp33 - specifc CD8 + T cells in WT relative to DKO mice (Fig. 5C), with a trend in changes in absolute cell numbers, consistent with temporal data from peripheral blood (Fig. 5A).

This antibody stains approximately 50 % of NK cells, 30 - 40 % of CD4 + and CD8 + T cells and 15 - 30 % B cells by flow cytometry.

This suggests that DGKζ - deficient CD8 + T cells are more dependent on help from CD4 + T cells at limiting dilutions of anti-CD3 stimulation.

Tumors can suppress CD4 + T cell activity and CTL tumor lysis directly through secretion of immunosuppressive factors including TGF - β1 but also PGE - 2, and IL - 10.

Naive CD8 + T cell experiments were performed with 5 × 104 cells per stimulation.

Induction of a CD4 + T regulatory type 1 response by cyclooxygenase -2-overexpressing glioma.

Replicating her experiments in T cell - competent mice confirmed that both mouse models mount a robust CD8 + T cell response to Zika infection.

Experiments were performed to confirm that a significant number of corneal allografts underwent rejection in the absence of CD4 + T cells.

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.

Tumor - infiltrating CD8 + T cells with high CD39 expression exhibited features of exhaustion, such as reduced production of TNF and IL - 2 and expression of co-inhibitory receptors.

Vitamin D up - regulates the vitamin D receptor by protecting it from proteasomal degradation in human CD4 + T 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.

This study examined the role of CD4 + T cell - independent mechanisms of corneal allograft rejection.

Subsets of CD4 + T lymphocytes play pivotal roles both in initiating the inflammatory process, by secreting pro-inflammatory cytokines, and by preventing inflammation, in part by secreting regulatory cytokines such as IL - 10 and TGFβ.

BALB / c corneal allografts were transplanted to C57BL / 6 beige nude mice that received either CD8 − or CD8 + T cells from C57BL / 6 CD4 knockout (KO) mice that had rejected BALB / c corneal allografts.

Some of these T cells become «effectos» (the ones that have direct roles in the immune response, including helper functions for CD4 + T cells, and cytotoxic functions for CD8 + T cells), while other T cells differentiate into resting memory cells.

This is a powerful system to screen polyfunctional CD4 + and CD8 + T - cell - specific immune responses.

Additional CD4 + T cell types have been discovered, including those producing IL - 17 (Th17 cells), that likely participate in the induction of IBD.

However, some studies have demonstrated a role for CD8 + T cell - mediated rejection of skin and cardiac allografts (16, 17).

Together, these data indicate that DGKζ and Cbl - b may differentially regulate the threshold of cytokine production in CD8 + T cells.

They are the first group to globally analyze the different types of CD4 + T cells that HIV enters and manipulates.

A total of 4 × 105 purified CD8 + T cells in 100 μl of serum - free media were incubated with 5 μg / ml biotinylated anti-CD3 (2C11; BD Pharmingen) and anti-CD28 Abs (37.51; (BD Pharmingen) for 1 min at 37 °C followed by the addition of 25 μg / ml streptavidin (Thermo Fisher Scientific, Waltham, MA) for 0, 5, and 15 min.

Use of CXCR4 as a co-receptor is associated with a marked drop in CD4 + T - cell counts [19].

Selective deletion of antigen - specific CD8 + T cells by MHC class I tetramers coupled to the type I ribosome - inactivating protein saporin.

The ion channel TRPV1 regulates the activation and proinflammatory properties of CD4 + T cells.

To determine if this was also true for Cbl - b − / − and DKO T cells, we isolated naive CD8 + T cells from mice deficient in DGKζ, Cbl - b, or both, prior to stimulation with anti-CD3 (Fig. 3D — F).

Graphs show the frequency of IFN - γ effector CD8 + T cells.

To assess whether changes in T cell numbers within the tumors could be responsible for the observed differences in tumor size, we processed the spleen and tumors from mice and calculated percentages of CD4 + and CD8 + T cells.

Whereas acute CD8 + T cell effector responses are enhanced in DGKζ - deficient mice postinfection with intracellular pathogens, persistent memory formation is impaired, most dramatically when both DGKζ and DGKα, the other isoform of DGK that metabolizes DAG downstream of the TCR in T cells, are deleted (35, 36).

However, the absolute amount of IFN - γ did not completely normalize between DGKζ − / − and Cbl - b − / − CD8 + T cells.

«We found that HIV enters a specific type of CD4 + T cell very efficiently, but is not able to multiply itself in these cells.»

Both CD8 − and CD8 + T cells from CD4 KO corneal allograft rejector mice mediated corneal allograft rejection following adoptive transfer to nude mice.

Bogen B. Peripheral T cell tolerance as a tumor escape mechanism: deletion of CD4 + T cells specific for a monoclonal immunoglobulin idiotype secreted by a plasmacytoma.

The notion that CD4 + T cells might be the pivotal mediators of corneal graft rejection arose from studies demonstrating the close correlation between delayed - type hypersensitivity (DTH), a classical CD4 + T cell - mediated immune process, and corneal graft rejection in rodents (10, 11).

Daniel Speiser, Pedro Romero, and colleauges report the first demonstration in humans that a synthetic vaccine can rapidly elicit strong specific CD8 + T cell responses in a majority of patients.

Alex Huang and Drew Pardoll, with Elizabeth Jaffee and Hyam Levitsky at Johns Hopkins School of Medicine demonstrate tumor - associated antigen processing and presentation to CD8 + T cell by bone marrow - derived professional antigen presenting cells via «cross-priming.»