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.

Slides:

Advertisements

Similar presentations

NK cells inhibited the expansion and function of ILC2s in vitro via IFN-γ. NK cells inhibited the expansion and function of ILC2s in vitro via IFN-γ. ILC2s.

Advertisements

Volume 45, Issue 2, Pages (August 2016)

IFN-γ and STAT1 are required for efficient induction of CXC chemokine receptor 3 (CXCR3) on CD4+ but not CD8+ T cells by Joseph Barbi, Steve Oghumu, Claudio.

Sustained Interactions between T Cell Receptors and Antigens Promote the Differentiation of CD4+ Memory T Cells Chulwoo Kim, Theodore Wilson, Kael F.

Volume 18, Issue 5, Pages (May 2003)

Volume 8, Issue 2, Pages (February 1998)

Hans-Peter Raué, Carol Beadling, Jennifer Haun, Mark K. Slifka

miR-150-Mediated Foxo1 Regulation Programs CD8+ T Cell Differentiation

Volume 23, Issue 1, Pages (April 2018)

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

Volume 11, Issue 6, Pages (June 2012)

Volume 31, Issue 1, Pages (July 2009)

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.

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

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.

TCF1 expression marks self-renewing human CD8+ T cells

Loss of DGKζ and Cbl-b results in a greater percentage of splenic CD8+ T cells with an activated phenotype. Loss of DGKζ and Cbl-b results in a greater.

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

Blimp-1 Transcription Factor Is Required for the Differentiation of Effector CD8+ T Cells and Memory Responses Axel Kallies, Annie Xin, Gabrielle T.

IRF4 is required for efficient Th1 CD4+ effector cell differentiation.

An Interleukin-21- Interleukin-10-STAT3 Pathway Is Critical for Functional Maturation of Memory CD8+ T Cells Weiguo Cui, Ying Liu, Jason S. Weinstein,

Volume 35, Issue 4, Pages (October 2011)

Volume 36, Issue 1, Pages (January 2012)

Volume 32, Issue 1, Pages (January 2010)

Volume 43, Issue 5, Pages (November 2015)

Volume 39, Issue 1, Pages (July 2013)

Volume 41, Issue 1, Pages (July 2014)

Volume 29, Issue 4, Pages (October 2008)

Volume 44, Issue 5, Pages (May 2016)

Volume 14, Issue 5, Pages (February 2016)

Volume 13, Issue 6, Pages (November 2015)

Matthew A. Williams, Eugene V. Ravkov, Michael J. Bevan Immunity

Volume 47, Issue 5, Pages e9 (November 2017)

Volume 27, Issue 2, Pages (August 2007)

Volume 32, Issue 1, Pages (January 2010)

Nonredundant antigen presentation by CD1c+ DCs infected with HIV and influenza virus. Nonredundant antigen presentation by CD1c+ DCs infected with HIV.

Volume 16, Issue 12, Pages (September 2016)

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.

Volume 40, Issue 2, Pages (February 2014)

Volume 38, Issue 6, Pages (June 2013)

Figure 4 Increased susceptibility of MIF−/− CD4+ T cells to immunosuppression by Dex in EAE (A) MOG35-55 peptide-activated donor cells from wild-type (Wt)

IRF4 is required for efficient Th1 CD4+ effector cell differentiation.

IRF4 expression is modulated by the signaling of IL-2 family cytokines

Volume 22, Issue 8, Pages (February 2018)

Antigen-specific immune responses are enhanced in hypertension.

APCs from hypertensive mice present antigens more efficiently.

Volume 35, Issue 4, Pages (October 2011)

Volume 25, Issue 4, Pages (April 2017)

LG NK cells appear to be conventional in phenotype.

Induction of IL-3–secreting CD4+ T cells.

Members of IL-1 family of cytokines favor the generation of IL-3–secreting CD4+ T cells in vitro. Members of IL-1 family of cytokines favor the generation.

CD8 T cell memory alters the immune profile in enhanced HLH without altering viral load. CD8 T cell memory alters the immune profile in enhanced HLH without.

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

c-Rel expression in donor T cells is increased after allo-HSCT.

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−/−

Volume 17, Issue 6, Pages (November 2016)

CD4+ memory T cells derived from either CD25hi or CD25lo effector cells respond robustly to secondary challenge. CD4+ memory T cells derived from either.

CD25 expression predicts effector and memory differentiation.

Mice with a B cell–specific loss of Ets1 have reduced marginal zone B cells and increased ASCs. (A) Flow cytometry analysis of CD21 versus CD23 in gated.

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.

TLR9 deficiency leads to more severe impairment of endothelium-dependent vasorelaxation and promotes aberrant B cell phenotype in imiquimod-induced autoimmunity.

Immune response of CEA-transgenic mice transferred with OT-1 splenocytes and immunized with ovalbumin and adjuvant. Immune response of CEA-transgenic mice.

LSECtin, expressed by B16 cells, inhibits the tumor-specific immune responses both in vivo and in vitro. LSECtin, expressed by B16 cells, inhibits the.

Supplementary Figure 1. The extrinsic acquisition of CD80 does not affect the cytotoxicity of Ag-specific memory CD8+ T cells. The LG and SP were obtained.

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.

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.

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

Immunization with IR or F/T elicits activated OT-I cells of distinct phenotypes. Immunization with IR or F/T elicits activated OT-I cells of distinct phenotypes.

Presentation transcript:

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 in the T cell compartment leads to a defect in the number of CD8+ memory precursor T cells during LCMV–Armstrong infection. WT and Runx2fl/fl mice were infected with LCMV–Armstrong and analyzed on days 9, 14, and 28 postinfection. (A) Gated CD8α+ splenocytes were stained for H2-Db gp33–41 tetramer and CD44. (B) Compilation of data shows total number of H2-Db gp33–41–specific splenocytes in WT versus Runx2fl/fl mice at days 9, 14, and 28 postinfection. (C) KLRG1 versus CD127 staining of WT and Runx2fl/fl CD8α+ CD44hi and H2-Db gp33–41 tetramer+ splenocytes at days 9, 14, and 28 postinfection. (D and E) Total number of H2-Db gp33–41–specific TECs (D) and MPCs (E) in WT versus Runx2fl/fl mice at days 9, 14, and 28 postinfection. (F) Cells were restimulated with gp33–41 peptide for 4 h in vitro. Total number of H2-Db gp33–41–specific IFN-γ+, TNF-α+, and IL-2+ splenocytes (triple producers) in WT versus Runx2fl/fl CD8α+ and CD44hi cells at days 9, 14, and 28 after LCMV–Armstrong infection. (G) WT C57/BL6 mice were infected with LCMV–Armstrong and analyzed on day 9 postinfection for Runx2 expression levels in CD8α+, CD44hi H2-Db gp33–41, gp276–286, and np396–404–specific MPCs versus TECs. (H) Normalized mean fluorescence intensity (MFI) of Eomes, TCF-1, and T-bet in H2-Db gp33–41 tetramer–specific WT versus Runx2fl/fl splenocytes were analyzed at days 9, 14, and 28 after LCMV–Armstrong infection by staining for Eomes, TCF-1, or T-bet. Data show normalized MFI for transcription factor staining in gated CD8α+ and CD44hi H2-Db gp33–41 tetramer+ cells. Samples were normalized to average MFI value for each protein in the WT samples in each experiment. Data are from three independent experiments with a total of 9–12 mice per group per time point. Data from (F) are from two independent experiments with a total of 12 mice. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001. ns, p > 0.05. Elizabeth Olesin et al. ImmunoHorizons 2018;2:251-261 Copyright © 2018 The Authors