Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. (A)

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MP cells are generated from naïve cells in the periphery.

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Volume 136, Issue 4, Pages (April 2009)

Enhancement of Treg suppressive function by allosteric modification of TIP60. Enhancement of Treg suppressive function by allosteric modification of TIP60.

Impaired development of Treg cell function upon overexpression of FOXP3A384T in naïve CD4+CD25− T cells. Impaired development of Treg cell function upon.

LV DNA, genome, and capsid are not required for DC activation and CD8+ T cell priming in vivo. LV DNA, genome, and capsid are not required for DC activation.

Specific depletion of TFH and LCMV-specific CD4 T cells.

Sialylated Ab-ICs promote enhanced humoral immune responses.

VLPs activate DCs and antigen-specific CD8+ T cells via the STING and cGAS pathway. VLPs activate DCs and antigen-specific CD8+ T cells via the STING and.

MP cells established in Rag γc KO mice are Toxoplasma antigen–unspecific T-bet+ population. MP cells established in Rag γc KO mice are Toxoplasma antigen–unspecific.

KIR2DS2 recognizes the HCV peptide LNP.

PKA phosphorylates Thr63 and Ser692 to increase HIF-1α stability.

LV pseudotransduction delivers proteins and activates DCs.

Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. (A)

LV activation of DCs and subsequent CD8+ T cell priming are dependent on STING and cGAS but not on MyD88, TRIF, or MAVS. LV activation of DCs and subsequent.

Protein sequence alignment of the NS3 helicase–encoding region of 63 flaviviruses demonstrates conservation of a KIR2DS2-binding peptide. Protein sequence.

Human PBMC-derived MERS-CoV–specific T cells are multifunctional.

Arp2/3-mediated formation of nuclear actin networks is essential for CD4+ T cell effector functions. Arp2/3-mediated formation of nuclear actin networks.

LNP activates KIR2DS2+, but not KIR2DL2+, NK cells.

Reduced FOXO1 expression in GC B cells from mice lacking regulatory CD4+ T cell–derived IL-10. Reduced FOXO1 expression in GC B cells from mice lacking.

Target cell lysis by ZnT8186–194-reactive CD8+ T cell clones.

Comparison of repertoire distributions to baseline.

Tfr cells robustly secrete IL-10 after acute viral infection.

Differential expression of TRM markers by donor- and recipient-derived T cells with time. Differential expression of TRM markers by donor- and recipient-derived.

Differentiation of AZD4785 from MAPK pathway inhibitors in vitro

Protein sequence alignment of the NS3 helicase–encoding region of 63 flaviviruses demonstrates conservation of a KIR2DS2-binding peptide. Protein sequence.

BAP1 deficiency results in thymic atrophy and loss of thymocyte populations. BAP1 deficiency results in thymic atrophy and loss of thymocyte populations.

Deubiquitinating activity, but not HCF-1 binding, is required for BAP1 function in thymocytes. Deubiquitinating activity, but not HCF-1 binding, is required.

MP cells are generated from naïve cells in the periphery.

CXCR5+/+ TFH cells are essential for the generation of LCMV-neutralizing antibodies and clearance of a persistent LCMV infection. CXCR5+/+ TFH cells are.

Cell viability tests. Cell viability tests. SEM images of (A) MC3T3-E1 cells and (B) MSCs on days 1, 3, and 5 of culture. (C) Survival rates of MC3T3-E1.

Microrobots with different cell-carrying capacities under different grid lengths (lg) and burr lengths (lb). Microrobots with different cell-carrying capacities.

CD4+CLA+CD103+ T cells in skin and blood are clonally related.

Immune evasion occurs through loss of TNF, IFN-γ, or antigen presentation pathways. Immune evasion occurs through loss of TNF, IFN-γ, or antigen presentation.

MR1T clones with distinct TCR usage display differential recognition of discrete activating ligands. MR1T clones with distinct TCR usage display differential.

RAPTOR deficiency impairs the DN-to-DP transition in αβ T cell development. RAPTOR deficiency impairs the DN-to-DP transition in αβ T cell development.

Dynamic regulation of cell metabolism and mTORC1 activity and the requirement of RAPTOR in thymocyte development. Dynamic regulation of cell metabolism.

MR1Ts recognized by the hpMR1+EC tetramer are more likely to be TRAV1-2−. MR1Ts recognized by the hpMR1+EC tetramer are more likely to be TRAV1-2−. PBMCs.

MYC degradation screen identifies a compound that stabilizes MYC protein. MYC degradation screen identifies a compound that stabilizes MYC protein. (A)

Loss of BAP1 blocks T cell differentiation at the DN3 stage in vitro.

Fig. 3. Increased expression of exhaustion markers and apoptosis markers on CAR8 cells in the presence of TCR antigen. Increased expression of exhaustion.

Overview of DS-A*02:01 production and usage for affinity measurements.

Fig. 3 BMS blocks functional responses in primary immune cells driven by IL-23 and IL-12. BMS blocks functional responses in primary immune.

Fig. 6 RUNX/CBFB interaction inhibitor, Ro5-3335, significantly decreases mouse neurofibroma growth in vivo. RUNX/CBFB interaction inhibitor, Ro5-3335,

Functional analysis of PVY CP N- and C-terminal deletions in planta

Enhancement of Treg suppressive function by allosteric modification of TIP60. Enhancement of Treg suppressive function by allosteric modification of TIP60.

MR1Ts respond to microbially derived ligands loaded on hpMR1 tetramers

Fig. 5 Simultaneous absence of caspase-3 and -7 is required for significant decrease of caspase-8 and -9 activation in intrinsic apoptosis. Simultaneous.

Fig. 2 Phenotypic analyses of Bcl11b-deficient Treg cells.

PD and efficacy of AZD4785 in KRAS mutant lung cancer xenograft models

Fig. 3 Prophylactic or therapeutic use of DECON protects from herpes infections in vitro. Prophylactic or therapeutic use of DECON protects from herpes.

GPR55 regulates γδT cell egress from PP and homing of gut-tropic CD8 T cells to the small intestine. GPR55 regulates γδT cell egress from PP and homing.

Separation-of-function mutations in ATM dictate responses to DNA damage and oxidative stress. Separation-of-function mutations in ATM dictate responses.

Initial testing and characterization of cAMPr in ES cells.

Chronic Treg reduction exacerbates bleomycin-induced skin fibrosis.

Human basophils are unresponsive to contact-dependent or contact-independent inhibition by Tregs. Human basophils are unresponsive to contact-dependent.

Fig. 3 Effects of ASO and eGLP1-ASO conjugates on gene expression and protein levels in vitro in cell lines and primary mouse islet cells. Effects of ASO.

Fig. 2 BX795 is nontoxic to HCE cells at therapeutic concentration.

NE cleaves and activates GSDMD.

Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice. Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice.

Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

Regulation of antibacterial B cell responses in the peritoneal cavity via MyD88 signaling in FRCs. Regulation of antibacterial B cell responses in the.

Fig. 3 Superiority of BAFF-R versus CD19-CAR T cells in a Burkitt lymphoma model is not due to greater tumor antigen density. Superiority of BAFF-R versus.

Acute circadian disruption alters ILC3 cytokine secretion.

REV-ERBα deficiency reduces frequency and number of NKp46+ ILC3s.

TNF-dependent communication between FALC FRCs and myeloid cells.

Circadian gene expression in ILC3s is associated with rhythmic cytokine expression. Circadian gene expression in ILC3s is associated with rhythmic cytokine.

γδ T cells producing IL-17 are required for short-term memory.

Fig. 4 MxB intermolecular assembly interfaces and their role in the MxB assembly and HIV-1 inhibition. MxB intermolecular assembly interfaces and their.

Fig. 1 Anti-LtxA antibody concentrations in various patient groups.

CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis. CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis.

Presentation transcript:

Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. Endogenously presented LNP is recognized by KIR2DS2 in the context of HCV. (A) HUH7 cells expressing the N17 (JFH1ΔE1E2-luc) replicon with (right) or without (left) HLA-C*0102 were co-incubated with NKL, NKL-2DL2, or NKL-2DS2 cells at the indicated E/T ratios. Luciferase activity from the cocultures was measured and normalized to expression in the absence of NKL cells. The relative inhibition of replication was then measured. The means and SEs of three experiments performed in duplicate are shown. Comparisons for NKL-2DS2 with NKL-2DL2 are indicated. (B) Replication of wild-type (WT) N17 (JFH1ΔE1E2-luc) replicon RNA or variants in which the LNP epitope had been mutated to aspartate at residues 3, 7, 8, and 9 (P3D, A7D, T8D, and L9D, respectively). As a nonreplicating control (Control), the N17 replicon carrying the lethal GND mutation in the viral NS5B protein was used. RLU, relative light units. (C) NKL, NKL-2DL2, or NKL-2DS2 cells were cocultured with HUH7-C*0102 cells expressing either wild-type or the L9D mutant HCV replicon. Luciferase activity was measured and plotted as percentage inhibition of viral RNA replication compared with HUH7 cells incubated in the absence of NKL cells. The means and SEs of three experiments performed in duplicate and P values for comparisons between NKL-2DS2 and NKL-2DL2 are shown. (D) NKL, NKL-2DL2, or NKL-2DS2 cells were cocultured with HUH7-C*0304 cells expressing either wild-type (left) or the L9D mutant HCV replicon (right). The percentage inhibition of replication compared with the no NKL control is shown. Statistical analyses for (A), (C), and (D) were performed using independent two-tailed t tests to compare NKL-2DS2 and NKL-2DL2. (E and F) 721:C*0304:ICP47 cells were loaded with the indicated peptides at saturating concentrations (100 μM) and then stained for HLA-C expression using the DT9 antibody (E) or the KIR2DS2–phycoerythrin (PE) tetramer (F). One representative histogram plot from three independent experiments is shown for each peptide, and the median fluorescence intensity of staining was indicated. Dark lines indicate peptide staining compared with the no peptide control (gray lines). (G) Western blot for phospho-Vav1 and Vav1 from 721.221:C*0304:ICP47 cells cultured with 20 μM of the indicated peptide and co-incubated with NKL-2DS2 cells at an E/T ratio of 1:1. One representative blot is shown together with densitometry of the phospho-Vav1/Vav1 ratio (mean ± SD) from three independent experiments. Statistical analysis was performed using one-way ANOVA, with Dunnett’s test for multiple comparisons (*P < 0.05, **P < 0.01, ***P < 0.001). Mohammed M. Naiyer et al. Sci. Immunol. 2017;2:eaal5296 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works