Baminercept

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Jaya Goyal - One of the best experts on this subject based on the ideXlab platform.

  • Baminercept treatment lowered RNA expression of the monocyte-associated gene SIGLEC1 in the blood.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Expression of the monocyte associated gene SIGLEC1 (qPCR determination) is elevated in patients with an elevated IFN signature (qPCR IFN score cut point of 1). b.) SIGLEC1 expression (log2) was reduced by treatment with Baminercept (n’s and boxes as per figure 4). P values are from a Mann-Whitney test of placebo vs. Baminercept treated patients.

  • Blockade of the lymphotoxin-LIGHT pathway with Baminercept reduces the blood RNA IFN signature in RA patients.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Analysis of the individual baseline IFN scores as determined using the 15 gene microarray data and a three-gene qPCR score showing excellent correlation. b). Analysis of the change in the 3-gene qPCR IFN score as a function of baseline IFN score following 14 weeks of treatment with 200 mg Baminercept q2w in TNF-IR patients, significance is calculated using a linear model of change in IFN score as an interaction of baseline IFN score and treatment (placebo or Baminercept). The significance for baseline IFN is p = 2×10−7 and for the interaction term p = 2.3×10−7. Treatment alone is marginally significant p = 0.0506. c). Change in the qPCR-based IFN score at 14 weeks in patients with low vs. high baseline IFN scores (low 1). Red boxes represent Baminercept (Bam) treated patients receiving either 70 or 200 mg q2w (DMARD-IR) or 200 mg q2w (TNF-IR) while black boxes indicate placebo treated patients; n = 20, 50, 11 and 12 (TNF-IR) and 49, 44, 50, 20, 28, 18 and 38 (DMARD-IR) patients in each category in the order listed. P values are from a Mann-Whitney test of placebo vs. Baminercept treated patients.

  • Flow diagrams for the two clinical trials assessing the effects of Baminercept treatment on rheumatoid arthritis patients.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    Flow diagrams for the two clinical trials assessing the effects of Baminercept treatment on rheumatoid arthritis patients.

  • IFN signature positive RA patients are lymphopenic and Baminercept treatment resulted in lymphocytosis.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Patients were segregated based on low and high microarray IFN scores (−4.5) and baseline blood lymphocyte counts are plotted. b). Time course of the effects on absolute lymphocyte counts during 14 weeks of Baminercept or placebo treatment (means, +/− SEM). All time points in two highest dosed cohorts in DMARD-IR were significant (p

  • Baminercept induced changes in total blood RNA expression.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    Heat map showing the change in gene expression after 14 week of either placebo or Baminercept treatment. Patients were forced into 4 groups based on treatment and baseline IFN signature. Each of the three gene clusters defined from initial unsupervised clustering are presented separately. The three clusters are characterized by genes associated with B cells, IFN response or NK cells, although some other genes are also present within each category. List only includes genes whose changes were significant (p

Evan Beckman - One of the best experts on this subject based on the ideXlab platform.

  • Baminercept treatment lowered RNA expression of the monocyte-associated gene SIGLEC1 in the blood.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Expression of the monocyte associated gene SIGLEC1 (qPCR determination) is elevated in patients with an elevated IFN signature (qPCR IFN score cut point of 1). b.) SIGLEC1 expression (log2) was reduced by treatment with Baminercept (n’s and boxes as per figure 4). P values are from a Mann-Whitney test of placebo vs. Baminercept treated patients.

  • Blockade of the lymphotoxin-LIGHT pathway with Baminercept reduces the blood RNA IFN signature in RA patients.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Analysis of the individual baseline IFN scores as determined using the 15 gene microarray data and a three-gene qPCR score showing excellent correlation. b). Analysis of the change in the 3-gene qPCR IFN score as a function of baseline IFN score following 14 weeks of treatment with 200 mg Baminercept q2w in TNF-IR patients, significance is calculated using a linear model of change in IFN score as an interaction of baseline IFN score and treatment (placebo or Baminercept). The significance for baseline IFN is p = 2×10−7 and for the interaction term p = 2.3×10−7. Treatment alone is marginally significant p = 0.0506. c). Change in the qPCR-based IFN score at 14 weeks in patients with low vs. high baseline IFN scores (low 1). Red boxes represent Baminercept (Bam) treated patients receiving either 70 or 200 mg q2w (DMARD-IR) or 200 mg q2w (TNF-IR) while black boxes indicate placebo treated patients; n = 20, 50, 11 and 12 (TNF-IR) and 49, 44, 50, 20, 28, 18 and 38 (DMARD-IR) patients in each category in the order listed. P values are from a Mann-Whitney test of placebo vs. Baminercept treated patients.

  • Flow diagrams for the two clinical trials assessing the effects of Baminercept treatment on rheumatoid arthritis patients.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    Flow diagrams for the two clinical trials assessing the effects of Baminercept treatment on rheumatoid arthritis patients.

  • IFN signature positive RA patients are lymphopenic and Baminercept treatment resulted in lymphocytosis.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Patients were segregated based on low and high microarray IFN scores (−4.5) and baseline blood lymphocyte counts are plotted. b). Time course of the effects on absolute lymphocyte counts during 14 weeks of Baminercept or placebo treatment (means, +/− SEM). All time points in two highest dosed cohorts in DMARD-IR were significant (p

  • Baminercept induced changes in total blood RNA expression.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    Heat map showing the change in gene expression after 14 week of either placebo or Baminercept treatment. Patients were forced into 4 groups based on treatment and baseline IFN signature. Each of the three gene clusters defined from initial unsupervised clustering are presented separately. The three clusters are characterized by genes associated with B cells, IFN response or NK cells, although some other genes are also present within each category. List only includes genes whose changes were significant (p

Tatiana Plavina - One of the best experts on this subject based on the ideXlab platform.

  • Baminercept treatment lowered RNA expression of the monocyte-associated gene SIGLEC1 in the blood.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Expression of the monocyte associated gene SIGLEC1 (qPCR determination) is elevated in patients with an elevated IFN signature (qPCR IFN score cut point of 1). b.) SIGLEC1 expression (log2) was reduced by treatment with Baminercept (n’s and boxes as per figure 4). P values are from a Mann-Whitney test of placebo vs. Baminercept treated patients.

  • Blockade of the lymphotoxin-LIGHT pathway with Baminercept reduces the blood RNA IFN signature in RA patients.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Analysis of the individual baseline IFN scores as determined using the 15 gene microarray data and a three-gene qPCR score showing excellent correlation. b). Analysis of the change in the 3-gene qPCR IFN score as a function of baseline IFN score following 14 weeks of treatment with 200 mg Baminercept q2w in TNF-IR patients, significance is calculated using a linear model of change in IFN score as an interaction of baseline IFN score and treatment (placebo or Baminercept). The significance for baseline IFN is p = 2×10−7 and for the interaction term p = 2.3×10−7. Treatment alone is marginally significant p = 0.0506. c). Change in the qPCR-based IFN score at 14 weeks in patients with low vs. high baseline IFN scores (low 1). Red boxes represent Baminercept (Bam) treated patients receiving either 70 or 200 mg q2w (DMARD-IR) or 200 mg q2w (TNF-IR) while black boxes indicate placebo treated patients; n = 20, 50, 11 and 12 (TNF-IR) and 49, 44, 50, 20, 28, 18 and 38 (DMARD-IR) patients in each category in the order listed. P values are from a Mann-Whitney test of placebo vs. Baminercept treated patients.

  • Flow diagrams for the two clinical trials assessing the effects of Baminercept treatment on rheumatoid arthritis patients.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    Flow diagrams for the two clinical trials assessing the effects of Baminercept treatment on rheumatoid arthritis patients.

  • IFN signature positive RA patients are lymphopenic and Baminercept treatment resulted in lymphocytosis.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Patients were segregated based on low and high microarray IFN scores (−4.5) and baseline blood lymphocyte counts are plotted. b). Time course of the effects on absolute lymphocyte counts during 14 weeks of Baminercept or placebo treatment (means, +/− SEM). All time points in two highest dosed cohorts in DMARD-IR were significant (p

  • Baminercept induced changes in total blood RNA expression.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    Heat map showing the change in gene expression after 14 week of either placebo or Baminercept treatment. Patients were forced into 4 groups based on treatment and baseline IFN signature. Each of the three gene clusters defined from initial unsupervised clustering are presented separately. The three clusters are characterized by genes associated with B cells, IFN response or NK cells, although some other genes are also present within each category. List only includes genes whose changes were significant (p

Alice Thai - One of the best experts on this subject based on the ideXlab platform.

  • identification of novel cd4 t cell subsets in the target tissue of sjogren s syndrome and their differential regulation by the lymphotoxin light signaling axis
    Journal of Immunology, 2016
    Co-Authors: Scott Haskett, Jian Ding, Wei Zhang, Alice Thai, Patrick Cullen, Britta Petersen, Galina Kuznetsov, Luke Jandreski, Stefan Hamann, Taylor L Reynolds
    Abstract:

    Despite being one of the most common rheumatologic diseases, there is still no disease-modifying drug for primary Sjogren’s syndrome (pSS). Advancing our knowledge of the target tissue has been limited by the low dimensionality of histology techniques and the small size of human salivary gland biopsies. In this study, we took advantage of a molecularly validated mouse model of pSS to characterize tissue-infiltrating CD4+ T cells and their regulation by the lymphotoxin/LIGHT signaling axis. Novel cell subsets were identified by combining highly dimensional flow and mass cytometry with transcriptomic analyses. Pharmacologic modulation of the LTβR signaling pathway was achieved by treating mice with LTβR-Ig, a therapeutic intervention currently being tested in pSS patients (Baminercept trial [NCT01552681][1]). Using these approaches, we identified two novel CD4+ T cell subsets characterized by high levels of PD1: Prdm1 + effector regulatory T cells expressing immunoregulatory factors, such as Il10 , Areg , Fgl2 , and Itgb8 , and Il21 + effector conventional T cells expressing a pathogenic transcriptional signature. Mirroring these observations in mice, large numbers of CD4+PD1+ T cells were detected in salivary glands from Sjogren’s patients but not in normal salivary glands or kidney biopsies from lupus nephritis patients. Unexpectedly, LTβR-Ig selectively halted the recruitment of PD1− naive, but not PD1+, effector T cells to the target tissue, leaving the cells with pathogenic potential unaffected. Altogether, this study revealed new cellular players in pSS pathogenesis, their transcriptional signatures, and differential dependency on the lymphotoxin/LIGHT signaling axis that help to interpret the negative results of the Baminercept trial and will guide future therapeutic interventions. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT01552681&atom=%2Fjimmunol%2F197%2F10%2F3806.atom

  • Baminercept treatment lowered RNA expression of the monocyte-associated gene SIGLEC1 in the blood.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Expression of the monocyte associated gene SIGLEC1 (qPCR determination) is elevated in patients with an elevated IFN signature (qPCR IFN score cut point of 1). b.) SIGLEC1 expression (log2) was reduced by treatment with Baminercept (n’s and boxes as per figure 4). P values are from a Mann-Whitney test of placebo vs. Baminercept treated patients.

  • Blockade of the lymphotoxin-LIGHT pathway with Baminercept reduces the blood RNA IFN signature in RA patients.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Analysis of the individual baseline IFN scores as determined using the 15 gene microarray data and a three-gene qPCR score showing excellent correlation. b). Analysis of the change in the 3-gene qPCR IFN score as a function of baseline IFN score following 14 weeks of treatment with 200 mg Baminercept q2w in TNF-IR patients, significance is calculated using a linear model of change in IFN score as an interaction of baseline IFN score and treatment (placebo or Baminercept). The significance for baseline IFN is p = 2×10−7 and for the interaction term p = 2.3×10−7. Treatment alone is marginally significant p = 0.0506. c). Change in the qPCR-based IFN score at 14 weeks in patients with low vs. high baseline IFN scores (low 1). Red boxes represent Baminercept (Bam) treated patients receiving either 70 or 200 mg q2w (DMARD-IR) or 200 mg q2w (TNF-IR) while black boxes indicate placebo treated patients; n = 20, 50, 11 and 12 (TNF-IR) and 49, 44, 50, 20, 28, 18 and 38 (DMARD-IR) patients in each category in the order listed. P values are from a Mann-Whitney test of placebo vs. Baminercept treated patients.

  • Flow diagrams for the two clinical trials assessing the effects of Baminercept treatment on rheumatoid arthritis patients.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    Flow diagrams for the two clinical trials assessing the effects of Baminercept treatment on rheumatoid arthritis patients.

  • IFN signature positive RA patients are lymphopenic and Baminercept treatment resulted in lymphocytosis.
    2014
    Co-Authors: Jadwiga Bienkowska, Alice Thai, Norm Allaire, Jaya Goyal, Tatiana Plavina, Ajay Nirula, Megan Weaver, Charlotte Newman, Michelle Petri, Evan Beckman
    Abstract:

    a). Patients were segregated based on low and high microarray IFN scores (−4.5) and baseline blood lymphocyte counts are plotted. b). Time course of the effects on absolute lymphocyte counts during 14 weeks of Baminercept or placebo treatment (means, +/− SEM). All time points in two highest dosed cohorts in DMARD-IR were significant (p

Henric Olsson - One of the best experts on this subject based on the ideXlab platform.

  • targeting non canonical nuclear factor κb signalling attenuates neovascularization in a novel 3d model of rheumatoid arthritis synovial angiogenesis
    Rheumatology, 2017
    Co-Authors: C X Maracle, Ae-ri Noort, P Kucharzewska, B Helder, Corine Van Der Horst, Pedro Correa De Sampaio, Katinka Pm Van Zoest, Arjan W Griffioen, Henric Olsson
    Abstract:

    OBJECTIVE: Angiogenesis is crucial in RA disease progression. Lymphotoxin β receptor (LTβR)-induced activation of the non-canonical nuclear factor-κB (NF-κB) pathway via NF-κB-inducing kinase (NIK) has been implicated in this process. Consequently, inhibition of this pathway may hold therapeutic potential in RA. We describe a novel three-dimensional (3D) model of synovial angiogenesis incorporating endothelial cells (ECs), RA fibroblast-like synoviocytes (RAFLSs) and RA synovial fluid (RASF) to further investigate the contributions of NF-κB in this process. METHODS: Spheroids consisting of RAFLSs and ECs were stimulated with RASF, the LTβR ligands LTβ and LIGHT, or growth factor bFGF and VEGF, followed by quantification of EC sprouting using confocal microscopy and digital image analysis. Next, the effects of anginex, NIK-targeting siRNA (siNIK), LTβR-Ig fusion protein (Baminercept) and a novel pharmacological NIK inhibitor were investigated. RESULTS: RASF significantly promoted sprout formation, which was blocked by the established angiogenesis inhibitor anginex (P < 0.05). LTβ and LIGHT induced significant sprouting (P < 0.05), as did bFGF/VEGF (P < 0.01). siNIK pre-treatment of ECs led to reductions in LTβR-induced vessel formation (P < 0.05). LTβR-Ig not only blocked LTβ- or LIGHT-induced sprouting, but also RASF-induced sprouting (P < 0.05). The NIK inhibitor blocked angiogenesis induced by LTβ, LIGHT, growth factors (P < 0.05) and RASF (P < 0.01). CONCLUSION: We present a novel 3D model of synovial angiogenesis incorporating RAFLSs, ECs and RASF that mimics the in vivo situation. Using this system, we demonstrate that non-canonical NF-κB signalling promotes neovascularization and show that this model is useful for dissecting relative contributions of signalling pathways in specific cell types to angiogenic responses and for testing pharmacological inhibitors of angiogenesis.

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