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.

Slides:



Advertisements
Similar presentations
High-dimensional analysis of lymphoid CD4+ T cells identified distinct TFH cell subsets in HIV+ patients and HCs. High-dimensional analysis of lymphoid.
Advertisements

Dominant IL-21 expression in TFH cells correlate with B cell pathology in HIV-infected LNs. Dominant IL-21 expression in TFH cells correlate with B cell.
Astrocytes Resist HIV-1 Fusion but Engulf Infected Macrophage Material
Identification of combination treatment–responsive effector/memory tumor-infiltrating CD8+ T cell population. Identification of combination treatment–responsive.
Identification of combination treatment–responsive dysfunctional tumor-infiltrating CD8+ T cell population. Identification of combination treatment–responsive.
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.
Impaired development of Treg cell function upon overexpression of FOXP3A384T in naïve CD4+CD25− T cells. Impaired development of Treg cell function upon.
CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. CD8α+ DC-deficient mice are highly susceptible to.
Nuclear Arp3 mediates formation of TCR-induced nuclear actin filaments
KIR2DS2 recognizes the HCV peptide LNP.
Astrocytes Resist HIV-1 Fusion but Engulf Infected Macrophage Material
Splenic CD169+ macrophages express a unique gene profile.
Viral fusion is required for DC activation.
Longitudinal analysis of ZIKV E–specific memory B cell responses in the DENV-experienced donors. Longitudinal analysis of ZIKV E–specific memory B cell.
LV pseudotransduction delivers proteins and activates DCs.
Regulatory CD4+ T cell–derived IL-10 is important for B cell differentiation and the GC response. Regulatory CD4+ T cell–derived IL-10 is important for.
CD169+ macrophages mediate Lm translocation to the splenic T cell zones. CD169+ macrophages mediate Lm translocation to the splenic T cell zones. (A) Confocal.
Improvement in the transcriptional activity of FOXP3A384T by enhancement of TIP60-FOXP3 interaction. Improvement in the transcriptional activity of FOXP3A384T.
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.
Cytosolic entry of Lm required for CD8α+ DC recruitment.
Virus-specific T cell responses are detected in all MERS survivors.
NRP1-expressing myeloid cells influence adipocyte hypertrophy, development of fatty liver, and CLSs. NRP1-expressing myeloid cells influence adipocyte.
VH usage of cross-reactive B cells induced by H5N1 or H7N9 vaccination
Nonredundant antigen presentation by CD1c+ DCs infected with HIV and influenza virus. Nonredundant antigen presentation by CD1c+ DCs infected with HIV.
Tfr cells robustly secrete IL-10 after acute viral infection.
DC subset cooperation for activation of antiviral T cells.
Characterization of the light-responsive transdermal MNs.
Donor and recipient BAL T cells are phenotypically and functionally memory T cells. Donor and recipient BAL T cells are phenotypically and functionally.
Differential expression of TRM markers by donor- and recipient-derived T cells with time. Differential expression of TRM markers by donor- and recipient-derived.
Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells. Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells.
Blood Tfr cells show expression of follicular and regulatory markers.
Persistent TCR–pMHC-I signaling drives the formation and maintenance of exhausted-like TRM cells. Persistent TCR–pMHC-I signaling drives the formation.
T-bethi MP cells produce IFN-γ in response to IL-12.
TCR signaling is required for exhausted-like TRM cell formation and maintenance. TCR signaling is required for exhausted-like TRM cell formation and maintenance.
Protein sequence alignment of the NS3 helicase–encoding region of 63 flaviviruses demonstrates conservation of a KIR2DS2-binding peptide. Protein sequence.
Murine gingival MSCs and skin MSCs produce and secrete IL-1RA–EV
Immune cell recruitment after the NIR-boosted and MN-mediated cancer immunotherapy. Immune cell recruitment after the NIR-boosted and MN-mediated cancer.
NCMs regulate T cell survival in TLOs via PD-L1.
PD-L1 selectively marks circulating NCMs.
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.
CD169+ macrophages mediate the transport of bacteria to T cell zones by trans-infecting CD8α+ DCs. CD169+ macrophages mediate the transport of bacteria.
Unique Fc functional profiling of HIV-specific Abs from neutralizers.
CD4+CLA+CD103+ T cells in skin and blood are clonally related.
Global analysis of RV[S/T]F motif phosphorylation during mitosis.
Shared phenotype of CD4+CLA+CD103+ T cells from human blood and skin.
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.
CD25 expression identifies two transcriptionally distinct subsets of very early effector cells. CD25 expression identifies two transcriptionally distinct.
Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs in vitro. Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs.
CD25 surface expression and TCR signal strength predict T helper differentiation and memory potential of early effector T cells in vivo. CD25 surface expression.
BMS blocks functional responses in primary immune cells driven by IFNα
Fig. 2 ODN enhances EV transfer between cells expressing TLR9.
CD25 expression predicts effector and memory differentiation.
Fig. 3 Prophylactic or therapeutic use of DECON protects from herpes infections in vitro. Prophylactic or therapeutic use of DECON protects from herpes.
Fig. 1 Prophylactic, neutralization, and therapeutic efficacy of HPAC.
Binding characteristics of mAbs isolated from plasmablasts during acute ZIKV infection. Binding characteristics of mAbs isolated from plasmablasts during.
IFN treatment of human midgestation villous explants induces syncytial knot formation. IFN treatment of human midgestation villous explants induces syncytial.
Human basophils are unresponsive to contact-dependent or contact-independent inhibition by Tregs. Human basophils are unresponsive to contact-dependent.
Impact of FRC-specific Myd88 ablation on omental FALC organization.
Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice. Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice.
Acute circadian disruption alters ILC3 cytokine secretion.
REV-ERBα deficiency reduces frequency and number of NKp46+ ILC3s.
REV-ERBα deficiency alters the epigenetic landscape and differentially affects clock gene expression in ILC3 subsets. REV-ERBα deficiency alters the epigenetic.
Circadian gene expression in ILC3s is associated with rhythmic cytokine expression. Circadian gene expression in ILC3s is associated with rhythmic cytokine.
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.
The neuropod cells. The neuropod cells. (Top left) Neuropod cells synapse with sensory neurons in the small intestine, as shown in a confocal microscopy.
Neutralizing activity of mAbs isolated from plasmablasts during acute ZIKV infection in DENV-experienced donors. Neutralizing activity of mAbs isolated.
Bb monocolonization enhances Treg population in the cLP.
Presentation transcript:

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 at the level of viral fusion. (A) HIV-1 fusion assay in blood DCs. Viral fusion revealed by CCF4 fluorescence in blood DCs after infection with HIV-1(BaL) (MOI = 0.8) or HIV-1(NL4-3) (MOI = 0.6) containing a BlaM-Vpr fusion protein. Fluorescence of the CCF4 product indicates viral fusion with target cells as a result of cleavage of the cell-loaded CCF4 substrate by the virus-contained BlaM. (B) Quantification as in (A) (n = 8 donors combined from four independent experiments). (C) Staining of GFP proteins contained in viral particles and CD44 in CD1c+ and CD141+ DCs after infection with HIV-1(V3R5) iGFP containing GAG-iGFP and GFP-Vpr fusion proteins, alone or in the presence of viral entry inhibitors MVC and TAK-779. Scale bars, 10 μm. (D) Quantification of the GFP density in GFPlow regions as in (C), shown for one representative donor (top) and average for five donors (bottom; combined from two independent experiments). (E) Levels of influenza virus receptors on blood DCs. SNA and MAA binding on CD1c+ and CD141+ DCs (representative of two independent experiments). (F) GFP expression in blood DC subsets that were sorted and infected for 48 hours with GFP-coding lenti(H1N1) Vpx at MOIGHOST X4R5 = 1 (n = 4 independent donors combined from two independent experiments). Viruses were not spinoculated. (G) Viral fusion revealed as in (A) by CCF4 fluorescence in blood DCs after infection with lenti(H1N1) (MOI = 1) containing a BlaM-Vpr fusion protein (n = 4 donors combined from two independent experiments). Viruses were not spinoculated. (H) GFP expression in blood DC subsets that were sorted and infected for 24 hours with HSV-1–GFP at MOI = 25 (one representative donor). (I) Quantification of GFP expression and frequency of live cells in blood DC subsets that were sorted and infected for 24 hours with HSV-1–GFP at MOI = 25 as in (H) (n = 10 combined from four experiments). (J) GFP expression in blood DC subsets that were sorted and infected for 24 hours with enhanced GFP–expressing VSV (VSVeGFP) at MOI = 16 (one representative donor). (K) Quantification of GFP expression and frequency of live cells in blood DC subsets that were sorted and infected for 24 hours with VSVeGFP at MOI = 16 as in (J) (n = 5 combined from two experiments). (L) Viral fusion revealed as in (A) by CCF4 fluorescence in blood DCs after infection with lenti(G) (MOI = 10) containing a BlaM-Vpr fusion protein (n = 13 combined from five experiments). ns, not significant; SSC, side scatter. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Aymeric Silvin et al. Sci. Immunol. 2017;2:eaai8071 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works