Memory CD8+ T cells that become terminally differentiated by multiple antigen encounters lose core 2 O-glycan synthesis activity. Memory CD8+ T cells that.

Slides:



Advertisements
Similar presentations
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.
Advertisements

MP cells, but not pathogen-elicited effector CD4+ T lymphocytes, rapidly produce IFN-γ during T. gondii infection independently of pathogen antigens. MP.
MP cells are generated from naïve cells in the periphery.
Expansion of Bacteroides species during colitis does not enhance TCR-specific T cell responses. Expansion of Bacteroides species during colitis does not.
LV envelope is responsible for DC activation.
Immunologic responses after the MN-mediated cancer immunotherapy.
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.
TPAD controller performance for three force components.
Three different types of transfer functions with a codomain of [0,1].
TPAD training protocol.
Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells. Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells.
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.
Core 2 O-glycan synthesis is stimulated by IL-15 signaling.
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.
Virus-specific T cell responses are detected in all MERS survivors.
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.
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.
Comparison of repertoire distributions to baseline.
Tfr cells robustly secrete IL-10 after acute viral infection.
Tfr cell–derived IL-10 is important for B cell differentiation and the GC response. Tfr cell–derived IL-10 is important for B cell differentiation and.
DC subset cooperation for activation of antiviral T cells.
Donor and recipient BAL T cells are phenotypically and functionally memory T cells. Donor and recipient BAL T cells are phenotypically and functionally.
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.
Definition of the cellular source of IL-22.
T-bethi MP cells produce IFN-γ in response to IL-12.
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.
Inhibiting or altering the timing of microbial antigen encounter results in inflammatory T cell responses against gut bacteria. Inhibiting or altering.
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.
Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. (A)
High numbers of non–islet-specific CTLs attenuate effector functions of islet-specific CTLs. High numbers of non–islet-specific CTLs attenuate effector.
BAP1 is required for homeostatic and antigen-driven expansion of peripheral T cells. BAP1 is required for homeostatic and antigen-driven expansion of peripheral.
Slc7a5 expression in preosteoclasts is reduced in ovariectomized mice.
CD4+CLA+CD103+T cells from human blood and skin share a functional profile. CD4+CLA+CD103+T cells from human blood and skin share a functional profile.
Shared phenotype of CD4+CLA+CD103+ T cells from human blood and skin.
MYC degradation screen identifies a compound that stabilizes MYC protein. MYC degradation screen identifies a compound that stabilizes MYC protein. (A)
CD25 expression identifies two transcriptionally distinct subsets of very early effector cells. CD25 expression identifies two transcriptionally distinct.
CD25 surface expression and TCR signal strength predict T helper differentiation and memory potential of early effector T cells in vivo. CD25 surface expression.
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 HRI regulates BCL11A levels.
Tfr cells respond better to immunization with self-antigens than with foreign antigens. Tfr cells respond better to immunization with self-antigens than.
Type I and III IFNR expression on hematopoietic cells is required for protection against IA. Type I and III IFNR expression on hematopoietic cells is required.
AEGIS autonomous targeting process.
Human Tfr cells do not express CD25.
Fig. 2 Regulation of CD73 and CD39 cell membrane expressions and extracellular adenosine levels by ERs in osteoprogenitor cells. Regulation of CD73 and.
CD4+ memory T cells derived from either CD25hi or CD25lo effector cells respond robustly to secondary challenge. CD4+ memory T cells derived from either.
Fig. 3 Regulation of CD73 and CD39 cell membrane expression and extracellular adenosine levels by ERs in osteoclasts. Regulation of CD73 and CD39 cell.
CD25 expression predicts effector and memory differentiation.
Colonic Treg TCRs react to MA Helicobacter species.
UNC drives MYC protein loss.
CAR expression promotes tonic activation of signaling networks.
Human basophils are unresponsive to contact-dependent or contact-independent inhibition by Tregs. Human basophils are unresponsive to contact-dependent.
IL-33 is not critical for initiation of allergic airways disease phenotype. IL-33 is not critical for initiation of allergic airways disease phenotype.
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.
Acute circadian disruption alters ILC3 cytokine secretion.
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.
In response to allergen, T cells and ILCs are equally important sources of IL-13. In response to allergen, T cells and ILCs are equally important sources.
T cell–derived IL-13 is essential for the inception of AHR.
Neutralizing activity of mAbs isolated from plasmablasts during acute ZIKV infection in DENV-experienced donors. Neutralizing activity of mAbs isolated.
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:

Memory CD8+ T cells that become terminally differentiated by multiple antigen encounters lose core 2 O-glycan synthesis activity. Memory CD8+ T cells that become terminally differentiated by multiple antigen encounters lose core 2 O-glycan synthesis activity. (A) Expression of CD62L and KLRG1 on primary and tertiary memory P14 CD8+ T cells 90 days after LCMV infection and (B) binding to E- and P-selectins. (C and D) Quantification of (B). (E) Expression of CD122 and CD132. (F and G) Quantification of (E). (H) Expression of total core 1 O-glycans (Jacalin) and unsialylated core 1 O-glycans (PNA). (I and J) Quantification of (H). (K) Primary and tertiary memory P14 CD8+ T cells were purified and stimulated with the indicated concentration of IL-15 for 15 min, and phosphorylation of STAT5 (Y694) was analyzed by immunoblot. (L) Primary and tertiary memory CD8+ T cells were purified and cultured with IL-15 for 3 days. Binding of MAL II, PNA, and the 1B11 antibody was analyzed. (M) Same as (L), except the glycosylation of PSGL-1 was analyzed by immunoblot. (N) Same as (L), except binding to E-selectin was analyzed by flow cytometry. (O) Quantification of (N) from four independent experiments. (P and Q) Same as (N) and (O), except for P-selectin. Jossef F. Osborn et al. Sci. Immunol. 2017;2:eaan6049 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works