LV pseudotransduction delivers proteins and activates DCs.

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Preferential infection of CD1c+ DCs by HIV-1, HIV-2, and influenza virus. Preferential infection of CD1c+ DCs by HIV-1, HIV-2, and influenza virus. (A)
LV envelope is responsible for DC activation.
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.
FIP200 deficiency alters mitochondria activation and ROS production in T cells. FIP200 deficiency alters mitochondria activation and ROS production in.
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.
Viral fusion is required for DC activation.
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.
Resistance of CD141+ DCs to influenza virus in vivo in humanized mice.
Resistance of CD141+ DCs to HIV and influenza virus infection at the level of viral fusion. Resistance of CD141+ DCs to HIV and influenza virus infection.
LNP activates KIR2DS2+, but not KIR2DL2+, NK cells.
Human cells produce type I and III IFNs upon Af stimulation.
Nonredundant antigen presentation by CD1c+ DCs infected with HIV and influenza virus. Nonredundant antigen presentation by CD1c+ DCs infected with HIV.
Enhanced expression of TLR7 protein in PBMCs from women.
β-Glucans do not modulate epithelial IL-33 or AHR.
DC subset cooperation for activation of antiviral T cells.
Macrophage-resident NRP1 mitigates cytokine release and proinflammatory polarization. Macrophage-resident NRP1 mitigates cytokine release and proinflammatory.
Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells. Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells.
Persistent TCR–pMHC-I signaling drives the formation and maintenance of exhausted-like TRM cells. Persistent TCR–pMHC-I signaling drives the formation.
TCR signaling is required for exhausted-like TRM cell formation and maintenance. TCR signaling is required for exhausted-like TRM cell formation and maintenance.
Dectin-1 is repressed in allergic individuals.
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.
Fig. 4 Labeling of Msmeg with DMN-Tre is fast and specific and depends on Ag85A function. Labeling of Msmeg with DMN-Tre is fast and specific and depends.
Fig. 2 AcPGP induces IL-8 and G-CSF release from human bronchial epithelial cells. AcPGP induces IL-8 and G-CSF release from human bronchial epithelial.
Antigen-specific immune responses are enhanced in hypertension.
LV particles and VLPs contain human genomic DNA recognized by the host STING pathway. LV particles and VLPs contain human genomic DNA recognized by the.
APCs from hypertensive mice present antigens more efficiently.
High numbers of non–islet-specific CTLs attenuate effector functions of islet-specific CTLs. High numbers of non–islet-specific CTLs attenuate effector.
Fig. 4. PVSRIPO infection of DCs is sublethal, is marginally productive, and induces sustained proinflammatory cytokine production. PVSRIPO infection of.
Shared phenotype of CD4+CLA+CD103+ T cells from human blood and skin.
Dectin-1 regulates innate IL-13.
Blood Tfr cells do not show specialized humoral regulatory capacity.
Dynamic regulation of cell metabolism and mTORC1 activity and the requirement of RAPTOR in thymocyte development. Dynamic regulation of cell metabolism.
IL-27 induces expression of multiple IR by CD8+ T cells.
RORα deficiency in Tregs results in exaggerated skin inflammation in response to EC sensitization. RORα deficiency in Tregs results in exaggerated skin.
Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs in vitro. Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs.
Fig. 1. Potent and selective down-regulation of KRAS mRNA and protein by AZD4785 in vitro and in vivo. Potent and selective down-regulation of KRAS mRNA.
Northern blot analysis of hY4 in CLL-derived exosomes and cells.
Fig. 3 BMS blocks functional responses in primary immune cells driven by IL-23 and IL-12. BMS blocks functional responses in primary immune.
BMS blocks functional responses in primary immune cells driven by IFNα
Fig. 4 Reconstitution of MCs in KitW-sh/W-sh mice increases IL-10+ Breg cells and suppresses the CHS response. Reconstitution of MCs in KitW-sh/W-sh mice.
Tfr cells respond better to immunization with self-antigens than with foreign antigens. Tfr cells respond better to immunization with self-antigens than.
Fig. 2 ODN enhances EV transfer between cells expressing TLR9.
TRPML1 is required for fast DC migration, chemotaxis, and arrival at the LNs. TRPML1 is required for fast DC migration, chemotaxis, and arrival at the.
Fig. 3 Proteomic analysis and Western blot analysis of protein cargos of various EVs. Proteomic analysis and Western blot analysis of protein cargos of.
Fig. 4 Cdc42 enhances the cellular uptake of EVs.
Fig. 5 Simultaneous absence of caspase-3 and -7 is required for significant decrease of caspase-8 and -9 activation in intrinsic apoptosis. Simultaneous.
Vaginal CD11c+ DCs from IL-17A−/− mice are impaired in potentiating Th17 responses because of diminished IL-1β production. Vaginal CD11c+ DCs from IL-17A−/−
Fig. 1 NDR2 facilitates RNA virus–induced IFN-β, IL-6, and TNF-α production via a kinase activity–independent mechanism in macrophages. NDR2 facilitates.
CD25 expression predicts effector and memory differentiation.
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.
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Fig. 2 Viperin promotes methionine oxidation of KSHV helicase.
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.
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.
IL-9–expressing TH cells are highly enriched in CCR4+/CCR8+ effector memory TH cells. IL-9–expressing THcells are highly enriched in CCR4+/CCR8+effector.
Fig. 5 IL-5–mediated signaling is critical for the development of CD1dintCD5+ Breg precursor cells and IL-10+ Breg cells. IL-5–mediated signaling is critical.
Circadian gene expression in ILC3s is associated with rhythmic cytokine expression. Circadian gene expression in ILC3s is associated with rhythmic cytokine.
Meningeal γδ T cell homeostasis is independent of inflammatory signals
Fig. 5 Treatment with molecules 13, 14, and 15 decreases HIV-1 R5 infection in human macrophages. Treatment with molecules 13, 14, and 15 decreases HIV-1.
Bb monocolonization enhances Treg population in the cLP.
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LV pseudotransduction delivers proteins and activates DCs. LV pseudotransduction delivers proteins and activates DCs. (A) Representative fluorescence-activated cell sorting (FACS) plots of mouse BMDCs that were treated with LV-GFP(V), LV-GFP(S), LPS, or no vector (NV) and analyzed for expression of GFP, CD86, and I-Ab. GFP geometric MFI was measured immediately after LV spin inoculation, and CD86 and I-Ab expression was measured 24 hours after LV treatment. (B) GFP, CD86, and I-Ab expression of LV-treated BMDCs was measured over 48 hours. (C) Representative FACS plots of mouse BMDCs, human moDCs, and 293T cells that were incubated with tenofovir (TFV; 40 μM), efavirenz (EFV; 80 μM), or no drug (ND) 6 hours before treatment with LV-GFP(V) and then analyzed 24 hours later. (D) Graph depicts the GFP MFI of BMDCs, moDCs, and 293T cells from (C). (E) Mouse BMDCs were incubated with or without cycloheximide (CHX; 50 μg ml−1) 1 hour before treatment with LV-GFP(V), and then, GFP MFI was presented relative to those BMDCs receiving no LV with or without cycloheximide. (F) Western blot analysis of GFP of lysates from LV-GFP(V) and LV expressing OVA pseudotyped with VSV-G [LV-OVA(V)] and purified GFP protein (40 ng). (G) Mouse BMDCs were treated as in (A) and analyzed for the amount of IL-6 and IL-12/23 in the supernatant by ELISA 24 hours after LV treatment. (H and I) Mouse BMDCs (H) and human moDCs (I) were treated as in (C) and analyzed for expression of CD86, I-Ab, or amount of IL-12/23 and/or IL-6 in the supernatant 24 hours after LV treatment. Data are representative of two (A to D and G to I) or three (E and F) independent experiments. Results are shown as mean ± SEM (B, D, E, G, and H). n.s., not significant. P > 0.05; ***P < 0.001 [one-way ANOVA (D and H) and unpaired Student’s t test (E and G)]. Jocelyn T. Kim et al. Sci. Immunol. 2017;2:eaal1329 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works