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

Slides:

Advertisements

Similar presentations

Activation of NK cells during the early stage of allergic and fibrotic lung inflammation. Activation of NK cells during the early stage of allergic and.

Advertisements

Enhanced ILC2 expansion after depletion of NK cells during the early stage of allergic and fibrotic lung inflammation. Enhanced ILC2 expansion after depletion.

Antitumor effect of the combination of IL-2 IC and anti–CTLA-4.

B-cell precursors in the spleen of Eμ-Myc mice are reduced by mTORC1 inhibition. B-cell precursors in the spleen of Eμ-Myc mice are reduced by mTORC1 inhibition.

Resveratrol modulates DSS-induced neutrophils during colitis.

Type 17 immunity is increased in STAT1−/− mice.

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.

Volume 14, Issue 5, Pages (May 2001)

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.

B-cell differentiation associates with down-regulation of vimentin expression. B-cell differentiation associates with down-regulation of vimentin expression.

Volume 18, Issue 4, Pages (April 2003)

Depo-Provera altered the expression of cell surface markers associated with HIV susceptibility. Depo-Provera altered the expression of cell surface markers.

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

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

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.

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

Altered cytokine production by Klrk1−/− NOD CTL

IL-21 is involved in the pathogenesis of EAM

CD160−/− mice have impaired clearance of oral L

Conditional deletion of MHC II on B cells does not regulate atherosclerotic plaque development in Ldlr−/− mice. Conditional deletion of MHC II on B cells.

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.

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

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.

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.

Mohamed A. Saleh et al. BTS 2016;1:

Both E12 and E47 Allow Commitment to the B Cell Lineage

TLR9 deficiency promotes aberrant T cell and myeloid dendritic cell (DC) phenotype in imiquimod-induced autoimmunity. TLR9 deficiency promotes aberrant.

CellTrace labeling of primary OT-I T cells allows for identification of OT-I nuclei after coculture. CellTrace labeling of primary OT-I T cells allows.

INKTcells/CD1d regulate intestinal immunity by controlling Treg induction iNKTcells/CD1d regulate intestinal immunity by controlling Treg induction ARegulatory.

Lipid presentation by CD11c+ cells controls iNKT cell subsets

LAT Links the Pre-BCR to Calcium Signaling

Fig. 5 Treatment with an OX40 agonist antibody of 3-week-old HBVtgRag−/− mice or mice with chronic HBV disease results in an altered immune response to.

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.

TCR signaling is required for exhausted-like TRM cell formation and maintenance. TCR signaling is required for exhausted-like TRM cell formation and maintenance.

BAP1 deficiency results in thymic atrophy and loss of thymocyte populations. BAP1 deficiency results in thymic atrophy and loss of thymocyte populations.

Rab27a promotes migration of neutrophils in vivo and in vitro.

Expression of transgenic IGF-1Ea propeptide in the skin increases local Treg cell numbers. Expression of transgenic IGF-1Ea propeptide in the skin increases.

Fig. 3 Intrarenal and RDLN lymphangiogenesis accompanied by lymphocyte expansion in the kidney, RDLN, and spleen. Intrarenal and RDLN lymphangiogenesis.

APCs from hypertensive mice present antigens more efficiently.

Inhibition of BCR activation by orthogonal inhibitors of SYK-AQL.

SYK activity is required for anti-IgM–induced DNA synthesis.

SYK activity is required for anti-IgM–induced CD86 expression.

CD8α+, CD8α−, and MoDCs from NOD.hCD205 mice express hCD205.

Generation and genotyping of Syk-AQL mice.

Representative flow cytometric plots showing different populations of dendritic cells and macrophages in the corneal stroma of mice with dry eye disease.

Fig. 4. Genetically engineered PD-L1

RAPTOR deficiency impairs the DN-to-DP transition in αβ T cell development. RAPTOR deficiency impairs the DN-to-DP transition in αβ T cell development.

Supplementation of c-Rel–competent Treg cells reverts exacerbated diabetes in c-Rel−/− NOD mice. Supplementation of c-Rel–competent Treg cells reverts.

Major hematopoietic cell populations in NOD mice are not affected by c-Rel deficiency. Major hematopoietic cell populations in NOD mice are not affected.

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.

Dynamic regulation of cell metabolism and mTORC1 activity and the requirement of RAPTOR in thymocyte development. Dynamic regulation of cell metabolism.

Induction of MHC-mismatched mixed chimerism depletes mature but not immature BM B cells by 60 days after HCT. Control and mixed chimeric NOD mice were.

Spontaneous and strong Tfh cell but not Tfr cell development in IL-2 KO mice. Spontaneous and strong Tfh cell but not Tfr cell development in IL-2 KO mice.

Loss of Tfh and GC B cells in 2KO-Bcl6TC mice.

Fig. 3 BMS blocks functional responses in primary immune cells driven by IL-23 and IL-12. BMS blocks functional responses in primary immune.

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.

BMS blocks functional responses in primary immune cells driven by IFNα

Reduced tumor growth in CCR5-deficient mice is associated with perturbed killing ability of Treg cells. Reduced tumor growth in CCR5-deficient mice is.

GC reaction is impaired in NOTCH2 knock-in mice.

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.

IL35 regulation of tumor growth is accompanied by suppression of CD4+ effector T-cell activity and expansion of Tregs. IL35 regulation of tumor growth.

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 Effector function of MIH5 isotype variants.

B-cell development in young Pax5+/− mice.

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

Meningeal γδ T cell homeostasis is independent of inflammatory signals

Effect on the recall response of Nrp1 deletion before infection.

Bb monocolonization enhances Treg population in the cLP.

Presentation transcript:

B cell development in wild-type and Syk-AQL mice. B cell development in wild-type and Syk-AQL mice. (A and B) Percentage of IgM+ (A) or IgD+ (B) lymphocytes present in mixed populations of splenocytes from wild-type (WT) versus Syk-AQL mice. Data represent means ± SEM for separate analyses of four mice. (C and D) An example of an analysis by flow cytometry comparing numbers of B220+IgM+ and IgM+IgD+ B cells present in a mixed splenocyte population isolated from a wild-type versus a Syk-AQL mouse. Wen-Horng Wang et al. ImmunoHorizons 2019;3:254-261 Copyright © 2019 The Authors