CD160−/− mice have impaired clearance of oral L

Slides:

Advertisements

Similar presentations

Volume 6, Issue 5, Pages (November 2009)

Advertisements

Depletion of CD169+ cells leads to increased expression of CD25 on enterotoxin A–specific Vβ3+ T cells. Depletion of CD169+ cells leads to increased expression.

Sunitinib plus rMVA–CEA–TRICOM vaccine decreased tumor burden and increased intratumoral infiltration of T lymphocytes in the MC38-CEA colon carcinoma.

PD-1 deficiency promotes the development of splenic GCs in male mice, and MR1 dissolves GCs in both genders. PD-1 deficiency promotes the development of.

Volume 42, Issue 5, Pages (May 2015)

Viral load and CD4+ T cells in CD8+ T cell–depleted YU-2–infected MISTRG mice. Viral load and CD4+ T cells in CD8+ T cell–depleted YU-2–infected MISTRG.

Changes in splenic CD4+ and CD8+ T cell subsets during acute and chronic HIV infection in MISTRG mice. Changes in splenic CD4+ and CD8+ T cell subsets.

Loss of Runx2 in the T cell compartment leads to a defect in the number of CD8+ memory precursor T cells during LCMV–Armstrong infection. Loss of Runx2.

TIGIT expression in naive T cells is accelerated by coculture with si-tolerant T cells at an early-stimulation stage. TIGIT expression in naive T cells.

Smaller T cell zone FRC areas in aged spleens.

False-color Raman images of CD4+T cells and CD8+ T cells from control and LPS-treated animals after day 1, 4, 10, and 30 obtained by k-means cluster analysis.

IL-10 treatment increases restorative macrophage (MΦ) bias and function in chronically infected skeletal muscle. IL-10 treatment increases restorative.

DKO CD8+ T cells demonstrate a strong effector response but altered memory differentiation and maintenance after LCMV infection. DKO CD8+ T cells demonstrate.

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

CD160−/− IELs have a defect in granzyme B production during L

Volume 7, Issue 2, Pages (February 2010)

Prf1−/− mice exhibit increased immunopathology with prior CD8 T cell memory secondary to immunization. Prf1−/− mice exhibit increased immunopathology with.

CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. CD8α+ DC-deficient mice are highly susceptible to.

Sustained HIV infection with CXCR4-tropic NL4-3 in MISTRG and MITRG mice. Sustained HIV infection with CXCR4-tropic NL4-3 in MISTRG and MITRG mice. Analogously.

Loss of pathogen-specific T cell memory is due to the absence of Runx2 in CD8+ T cells. Loss of pathogen-specific T cell memory is due to the absence of.

B-1a and B-1b Cells Exhibit Distinct Developmental Requirements and Have Unique Functional Roles in Innate and Adaptive Immunity to S. pneumoniae Karen.

CD169+ macrophages play a critical role in mediating innate immune cell reorganization. CD169+ macrophages play a critical role in mediating innate immune.

Specific depletion of CD4-DTR–derived CD4 T cells.

IL-21 is involved in the pathogenesis of EAM

CCR2+ monocytes are a relevant source of type I IFN in response to Af.

CD4 T cells are responsible for the intensified joint pathology at 6 d postinfection. CD4 T cells are responsible for the intensified joint pathology at.

Volume 6, Issue 5, Pages (November 2009)

CD169+ macrophages mediate Lm translocation to the splenic T cell zones. CD169+ macrophages mediate Lm translocation to the splenic T cell zones. (A) Confocal.

Saskia Hemmers, Alexander Y. Rudensky Cell Reports

Immune cell populations, activation, and NKG2D and H60a expression in the spleen of untreated and antibiotic-treated Klrk1+/+ and Klrk1−/− NOD mice. Immune.

IFN-γ induces TNF family ligand protein expression in vitro and in vivo. IFN-γ induces TNF family ligand protein expression in vitro and in vivo. (A and.

Inflammatory APC show highest expression of TNF superfamily ligands in the lung after LCMV infection. Inflammatory APC show highest expression of TNF superfamily.

A–E, Active avoidance (A–D) and optokinetic testing (E) in an independent cohort. A–E, Active avoidance (A–D) and optokinetic testing (E) in an independent.

Myung H. Kim, Elizabeth J. Taparowsky, Chang H. Kim Immunity

Lipid presentation by CD11c+ cells controls iNKT cell subsets

Volume 34, Issue 5, Pages (May 2011)

Volume 40, Issue 5, Pages (May 2014)

Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.

MP cells can mediate resistance in infectious models that induce TH1-type immunity. MP cells can mediate resistance in infectious models that induce TH1-type.

Ag 85A–specific immune responses.

IL-27 contributes to IR expression by lung T cells during toxoplasmosis. IL-27 contributes to IR expression by lung T cells during toxoplasmosis. (A) Il27p28-GFP.

EGFR activation in GCs inhibits GAP formation and luminal antigen delivery throughout life. EGFR activation in GCs inhibits GAP formation and luminal antigen.

The mucosal environment regulates CD160 expression on IELs

Expression of tomoregulin-1 in wild-type and cardiac hypertrophy mouse myocardium. Expression of tomoregulin-1 in wild-type and cardiac hypertrophy mouse.

The microbiota downregulate CD160 expression on IELs

Unchanged worm burden and microfilaremia in basophil-deficient mice compared with their basophil-competent littermates. Unchanged worm burden and microfilaremia.

NCMs regulate T cell survival in TLOs via PD-L1.

Comparison of male and female CD8+ T cells primed with different amounts of cognate Ag. (A) Schematic of experimental design: 1 × 104 gBT-I CD8+ T cells.

AhR activation reduces lung DC gene and surface expression of DC-SIGN.

CD160 on CD8+ T cells is required for optimal clearance of L

CD169+ macrophages mediate the transport of bacteria to T cell zones by trans-infecting CD8α+ DCs. CD169+ macrophages mediate the transport of bacteria.

B cell development in wild-type and Syk-AQL mice.

Anti-DNA Abs were not affected by the deletion of GCs in pristane-induced lupus model. Anti-DNA Abs were not affected by the deletion of GCs in pristane-induced.

CypD-deficient mice are susceptible to Mtb infection.

Increased pancreatic insulin content and islet size and protection against HFD- and palmitate-induced cell death in PKCδKN-overexpressing mice. Increased.

CD25 surface expression and TCR signal strength predict T helper differentiation and memory potential of early effector T cells in vivo. CD25 surface expression.

Overexpression of IL-27 upregulates expression of multiple IR by T cells in vivo. Overexpression of IL-27 upregulates expression of multiple IR by T cells.

Volume 19, Issue 6, Pages (May 2017)

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−/−

Local proliferation of infiltrating circulating memory T cells.

Mice with a B cell–specific deletion of Ets1 have increased memory phenotype B cells but no increase in switching to IgG1. Mice with a B cell–specific.

Bacterial antigen encounter occurs during a specific preweaning interval, is dependent on GCs, and correlates with the presence of colonic GAPs. Bacterial.

Mice with a B cell–specific deletion of Ets1 do not have increased CD4+ T cell activation. Mice with a B cell–specific deletion of Ets1 do not have increased.

E2 induces IL-17–producing γδ+ T cells in the FGT

Fig. 3 MCA-mediated neutrophil recruitment accelerates bacterial clearance in the skin. MCA-mediated neutrophil recruitment accelerates bacterial clearance.

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

Fetal-derived γδ T cells infiltrate the meninges from birth.

Bb monocolonization enhances Treg population in the cLP.

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:

CD160−/− mice have impaired clearance of oral L CD160−/− mice have impaired clearance of oral L. monocytogenes infection. CD160−/− mice have impaired clearance of oral L. monocytogenes infection. (A) Age-matched WT (blue circles, n = 7–16) and CD160−/− (red circles, n = 7–16) littermates were infected with 2 × 109L. monocytogenes orally, and bacterial burden from spleen, mLN, small intestine, and colon was assessed on day 3 postinfection. (B) Bacterial burden from small intestine and colon on day 7 after oral L. monocytogenes infection with 2 × 109L. monocytogenes from age-matched WT (blue circles, n = 14–17) and CD160−/− (red circles, n = 14–17) littermates. (C) Percentages of WT (n = 14–17) and CD160−/− (n = 14–17) littermates that cleared (cyan) versus those with detectable L. monocytogenes (green) in the small intestine and colon on day 7 after L. monocytogenes oral infection with 2 × 109L. monocytogenes. (D) Bacterial burden from spleen and mLN on day 7 after oral L. monocytogenes infection with 2 × 109L. monocytogenes from age-matched WT (blue circles, n = 10) and CD160−/− (red circles, n = 10) littermates. Age-matched RAG−/− (blue circles, n = 5–18) and CD160−/− RAG−/− (red circles, n = 7–18) littermates were infected with 2 × 109L. monocytogenes orally, and bacterial burden from spleen, mLN, and colon was assessed on (E) day 3 and (F) day 7 postinfection. Data are pooled from four independent experiments, (A), (C), and (D). Data are pooled from three independent experiments, (B), (E), and (F). Significance was assessed using Mann–Whitney nonparametric test in (A), (B), (D), and (E) and χ2 test in (C). Data are represented means ± SEM. **p < 0.01. Catherine L. Tan et al. ImmunoHorizons 2018;2:238-250 Copyright © 2018 The Authors