Figure 3 TRIF deficiency abrogates the immunomodulatory effects of glatiramer acetate treatment on cytokines and experimental autoimmune encephalomyelitis.

Slides:

Advertisements

Similar presentations

Molecular Therapy - Oncolytics

Advertisements

From: Effective Arrestin–Specific Immunotherapy of Experimental Autoimmune Uveitis with RTL: A Prospect for Treatment of Human Uveitis Trans. Vis. Sci.

Figure 5 Mononuclear cell subset isolation from spinal cord of mice with experimental autoimmune encephalomeylitis Mononuclear cell subset isolation from.

Molecular Therapy - Oncolytics

Figure 2 Anti-LINGO-1 (Li81) does not affect cytokine production

Volume 18, Issue 5, Pages (May 2010)

Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.

Effects of SC144 on in vivo ovarian tumor.

H31m1-PDL1 cells form progressively growing tumors in WT mice.

The Alarmin IL-33 Derived from HSV-2-Infected Keratinocytes Triggers Mast Cell- Mediated Antiviral Innate Immunity Rui Aoki, Tatsuyoshi Kawamura, Fumi.

Peritumoral injections of poly(I:C) induce type I IFN–dependent cytotoxic immunity and delay the growth of primary and transplanted Hgf-Cdk4R24C melanomas.

Figure 4 Abundance of cytokines which showed significant difference in expression in the plasma and the cultured PBMC of patients with RRMS Abundance of.

Figure 5 Cytokine release and stimulation of cells during alemtuzumab treatment Cytokine release and stimulation of cells during alemtuzumab treatment.

Figure 2 APCs from laquinimod-treated mice inhibit differentiation of Tfh cells APCs from laquinimod-treated mice inhibit differentiation of Tfh cells.

Figure 6 Laquinimod treatment of spontaneous EAE prevents progression and reduces the frequency of Tfh cells Laquinimod treatment of spontaneous EAE prevents.

Figure 1 Cytokine titers determined by the multiplex bead assay Plotted are cytokine titers (pg/mL) in CSF of patients with other noninflammatory neurologic.

Figure 2 Mean serum concentrations of BIIB033 vs time(A) Single ascending dose study and (B) multiple ascending dose study. Mean serum concentrations of.

Figure 1 Peripheral blood leukocyte subset counts during dimethyl fumarate treatmentComplete blood cell counts were obtained at baseline (n = 34) and at.

Figure 4 Glatiramer acetate treatment negatively regulates IFN-β production by targeting components of the IFN-β enhanceosome (A) Wild-type (WT) monocytes.

Figure 3 Responder subset (A) Percentage of “responders” (nonprogressing patients) at week 25 after 6 months of treatment; percentage of “responders” in.

Histological changes in mouse colons after DSS treatment.

Figure 2 Mononuclear cell numbers after enzymatic dissociation methods in mice with clinical experimental autoimmune encephalomyelitis Mononuclear cell.

Figure 1 Evolution of blood cell counts during 18-month treatment and follow-up (A) Mean white blood cell count, (B) mean lymphocyte count, (C) mean eosinophil.

Figure 4 Pattern of relapse in patients with MOG-Ab Five myelin oligodendrocyte glycoprotein antibody (MOG-Ab)–positive patients experienced a relapse,

Combination extract inhibits immune responses in vivo.

Volume 18, Issue 4, Pages (April 2010)

Figure 5 Increased B cell-activating factor (BAFF) levels are shared between immunomodulatory treatments Increased B cell-activating factor (BAFF) levels.

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

Volume 41, Issue 4, Pages (October 2014)

Volume 32, Issue 5, Pages (May 2010)

Figure 1 Fingolimod does not alter human monocyte viability Peripheral blood mononuclear cells from healthy donors were briefly exposed to increasing concentrations.

Figure 4 Laquinimod treatment suppresses development of spontaneous EAE Laquinimod treatment suppresses development of spontaneous EAE (A) 2D2 × Th mice.

Figure 4 Leukocyte subset isolation from brain tissue by enzymatic dissociation Leukocyte subset isolation from brain tissue by enzymatic dissociation.

Deficiency of TLR9 promotes more severe renal inflammation in imiquimod-induced autoimmunity. Deficiency of TLR9 promotes more severe renal inflammation.

Figure 4 Shared and unique immune changes induced by multiple sclerosis (MS) immunomodulatory treatments Shared and unique immune changes induced by multiple.

Figure 1 Annual trend in specimen type submitted as first sample for aquaporin-4 immunoglobulin G testing (serum only vs CSF only vs both) from 101,065.

Figure 5 ADP-induced inflammatory responses require P2Y12 receptors in human microgliaIncreasing concentrations of ADP (5, 50, and 200 μM) increased tumor.

(A) Serum CRP levels. (A) Serum CRP levels. T2DM: n=6 per group. *p

Figure 3 Cytokine gene expression in PBMC stimulated with PPD or MBP in vitroCytokine messenger RNA transcripts were isolated from peripheral blood mononuclear.

Figure 1 Association between serum levels of IL-18 and hippocampal volume in patients with schizophrenia Scatter plots show a positive correlation between.

Figure 3 Multiple sclerosis (MS) immunomodulatory treatments interferon-β (IFNB) and fingolimod (FTY720) result in global perturbation of the immune system.

Figure 1 Laquinimod treatment reduces the frequency of Tfh cells and IL-21–producing T cells in rMOG-induced EAE Laquinimod treatment reduces the frequency.

Figure 3 Laquinimod (LAQ) reduces microglia infiltration and acute axonal damage after 6 weeks of cuprizone Laquinimod (LAQ) reduces microglia infiltration.

Figure 2. Odds ratios (ORs) from the multivariate logistic regression analysis and hazard ratios (HRs) from the Cox regression analysis Odds ratios (ORs)

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)

Figure 4. The N:M ratio is significantly increased in patients with ALS and correlates with disease progression The N:M ratio is significantly increased.

Figure 2 Evolution of blood cell counts during interleukin (IL)–7 therapy Evolution of blood cell counts during interleukin (IL)–7 therapy The leukocyte.

Figure Avidity of IgG specific for influenza A and B following flu vaccinationAvidity of immunoglobulin (Ig) G specific for influenza A and B before and.

Figure 2 Glatiramer acetate treatment induced M2 differentiation through a MyD88-independent pathway (A) As described previously,3 M2 monocytes were treated.

Figure 2 Natalizumab increases expression of proinflammatory genes and cytokines by CD49d+ memory CD4 cells Natalizumab increases expression of proinflammatory.

Figure 1 Peripheral blood lymphocyte counts during dose titrationB-lymphocyte (CD19+; A) and total lymphocyte (CD45+; B) counts (cells/µL) in peripheral.

Figure 3 Impact of short-term MP administration on frequency and phenotype of slanDCs and monocytes in the blood of patients with MSThe percentages of.

Figure 2 Fingolimod impairs induction of activation markers on human monocytes Peripheral blood mononuclear cells from healthy donors were briefly exposed.

Figure 3 Downregulation of T-bet expression in brain-infiltrating MIF−/− CD4+ T cells Macrophage migration inhibitory factor (MIF)−/− and wild-type (Wt)

Figure 1 Classical pathway and lectin pathway activity in patients with multifocal motor neuropathy and controls Classical pathway (CP) activity (A) and.

Figure 2 B-cell very late antigen-4 (VLA-4) deficiency reduced CNS accumulation of B cells, but not proinflammatory or regulatory T cells (Treg), in myelin.

Figure 2 Effect of DMF therapy on the T helper cell repertoire and cytokine production Effect of DMF therapy on the T helper cell repertoire and cytokine.

Figure 3 Fingolimod inhibits TNF-α secretion by human monocytes Peripheral blood mononuclear cells from healthy donors were briefly exposed to increasing.

Yian Gu et al. Neurol Neuroimmunol Neuroinflamm 2019;6:e521

Gitanjali Das et al. Neurol Neuroimmunol Neuroinflamm 2018;5:e453

Figure 1 EAE severity and CNS pathology in Dex-treated MIF−/− and Wt mice Wild-type (Wt) and macrophage migration inhibitory factor (MIF)−/− mice were.

Figure 1 Tissue processing methods and cellular viability

Figure 2 Effect of Dex on cytokine production by MIF−/− or Wt T cells in EAE Wild-type (Wt) and macrophage migration inhibitory factor (MIF)−/− mice were.

Figure 5 TLR-dependent signaling pathways inhibited by glatiramer acetate Myeloid differentiation primary response gene 88 (MyD88) and Toll-IL-1 receptor.

Figure 2 Interleukin-6 concentrations in the CSF In 2 mutation carriers (patient 1 in dark blue triangle and patient 5 in light blue triangle carrying.

by Gonghua Huang, Yanyan Wang, Peter Vogel, and Hongbo Chi

Irradiated whole-cell vaccination with MOC1, but not MOC2, induces immunologic memory. Irradiated whole-cell vaccination with MOC1, but not MOC2, induces.

Figure 2. Percentage of CD16− monocytes in the blood is reduced during disease progression Percentage of CD16− monocytes in the blood is reduced during.

Figure 2 Segmented time series of median annual cost in the United States for first-generation multiple sclerosis disease-modifying therapies relative.

Toll-like receptors, adapter proteins, and signaling molecules.

Presentation transcript:

Figure 3 TRIF deficiency abrogates the immunomodulatory effects of glatiramer acetate treatment on cytokines and experimental autoimmune encephalomyelitis Wild-type (WT) and Toll-IL-1 receptor domain–containing adaptor inducing interferon-β (TRIF)–deficient mice treated with glatiramer acetate (GA) or vehicle (n = 5 mice/group) were injected IP with (A) lipopolysaccharide (LPS) (100 ng/kg) or (B) Pam3CSK4 (100 ng/kg). TRIF deficiency abrogates the immunomodulatory effects of glatiramer acetate treatment on cytokines and experimental autoimmune encephalomyelitis Wild-type (WT) and Toll-IL-1 receptor domain–containing adaptor inducing interferon-β (TRIF)–deficient mice treated with glatiramer acetate (GA) or vehicle (n = 5 mice/group) were injected IP with (A) lipopolysaccharide (LPS) (100 ng/kg) or (B) Pam3CSK4 (100 ng/kg). (C) Myeloid differentiation primary response gene 88 (MyD88)–deficient mice were injected IP with Poly(I:C) (10 μg/kg). Serum levels of tumor necrosis factor (TNF) and interleukin (IL)–6 were quantitated by ELISA 5 hours after injection. Results are presented as the mean ± SEM (n = 3) of 2 experiments that provided similar results; *p < 0.05, **p < 0.01, ***p < 0.001 as determined by Student t test. (D) On day 0, C57BL/6J WT (left) or TRIF-deficient mice (right) mice were immunized with MOG peptide (p35-55; 50 μg). GA (250 μg) was administered once (SC in incomplete Freund's adjuvant [IFA]) on the same day as immunization (day 0). Control mice received a single SC injection of IFA. For all experimental autoimmune encephalomyelitis experiments, mean disease score ±SEM is shown. *p < 0.05 as determined by Mann-Whitney U test. Results shown are representative of 3 independent experiments. Nicolas Molnarfi et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e179 © 2015 American Academy of Neurology