Jonathan Powell

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc A modified model of T-cell differentiation based on mTOR activity and metabolism
    Jonathan D Powell
    Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231
    Cold Spring Harb Symp Quant Biol 78:125-30. 2013
  2. pmc Egr3 induces a Th17 response by promoting the development of γδ T cells
    Rose M Parkinson
    The Sidney Kimmel Cancer Research Center, The Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 9:e87265. 2014
  3. pmc All PI3Kinase signaling is not mTOR: dissecting mTOR-dependent and independent signaling pathways in T cells
    Christopher J Gamper
    Department of Oncology, Johns Hopkins University Baltimore, MD, USA
    Front Immunol 3:312. 2012
  4. pmc Regulation of CD4⁺ and CD8⁺ effector responses by Sprouty-1
    Sam Collins
    Department of Medicine, Division of Pulmonary and Critical Care, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 7:e49801. 2012
  5. pmc The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2
    Greg M Delgoffe
    Sidney Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Nat Immunol 12:295-303. 2011
  6. pmc Hyaluronan fragments induce IFNβ via a novel TLR4-TRIF-TBK1-IRF3-dependent pathway
    Katharine E Black
    Department of Medicine, John Hopkins University School of Medicine, Baltimore, USA
    J Inflamm (Lond) 10:23. 2013
  7. pmc Regulation of immune responses by mTOR
    Jonathan D Powell
    Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Annu Rev Immunol 30:39-68. 2012
  8. pmc Fueling memories
    Jonathan D Powell
    Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Immunity 36:3-5. 2012
  9. pmc Anti-oxidant inhibition of hyaluronan fragment-induced inflammatory gene expression
    Michael Eberlein
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    J Inflamm (Lond) 5:20. 2008
  10. ncbi request reprint Dissecting the mechanism of T-cell anergy with immunophilin ligands
    Jonathan D Powell
    Department of Oncology Immunology Hematopoiesis, Johns Hopkins School of Medicine, 1650 Orleans St, CRB 443, Baltimore, MD 21231, USA
    Curr Opin Investig Drugs 7:1002-7. 2006

Research Grants

  1. A2a receptor engagement promotes T cell tolerance
    Jonathan D Powell; Fiscal Year: 2010
  2. INDUCTION AND MAINTENANCE OF T CELL ANERGY
    Jonathan Powell; Fiscal Year: 2002

Collaborators

Detail Information

Publications34

  1. pmc A modified model of T-cell differentiation based on mTOR activity and metabolism
    Jonathan D Powell
    Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231
    Cold Spring Harb Symp Quant Biol 78:125-30. 2013
    ..Such a model more readily explains the generation of effector and memory cells including the concept of effector and memory Foxp3(+) regulatory cells. ..
  2. pmc Egr3 induces a Th17 response by promoting the development of γδ T cells
    Rose M Parkinson
    The Sidney Kimmel Cancer Research Center, The Johns Hopkins School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 9:e87265. 2014
    ..Our data also demonstrates that the role played by Egr3 in T cell activation and differentiation is more complex than previously thought. ..
  3. pmc All PI3Kinase signaling is not mTOR: dissecting mTOR-dependent and independent signaling pathways in T cells
    Christopher J Gamper
    Department of Oncology, Johns Hopkins University Baltimore, MD, USA
    Front Immunol 3:312. 2012
    ..Importantly, what has become clear is that targeting both mTOR-dependent and mTOR-independent PI3K-induced signaling distally affords the opportunity for more selective regulation of T cell differentiation and function...
  4. pmc Regulation of CD4⁺ and CD8⁺ effector responses by Sprouty-1
    Sam Collins
    Department of Medicine, Division of Pulmonary and Critical Care, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America
    PLoS ONE 7:e49801. 2012
    ..These findings suggest that targeting Spry1 might prove to be a novel means of enhancing tumor immunotherapy...
  5. pmc The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2
    Greg M Delgoffe
    Sidney Kimmel Comprehensive Cancer Research Center, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Nat Immunol 12:295-303. 2011
    ..These findings define a previously unknown paradigm that links T cell differentiation with selective metabolic signaling pathways...
  6. pmc Hyaluronan fragments induce IFNβ via a novel TLR4-TRIF-TBK1-IRF3-dependent pathway
    Katharine E Black
    Department of Medicine, John Hopkins University School of Medicine, Baltimore, USA
    J Inflamm (Lond) 10:23. 2013
    ..HA fragments are known to induce inflammatory gene expression via TLR-MyD88-dependent pathways...
  7. pmc Regulation of immune responses by mTOR
    Jonathan D Powell
    Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Annu Rev Immunol 30:39-68. 2012
    ..In this review, we discuss the ability of mTOR to direct the adaptive immune response. Specifically, we focus on the role of mTOR in promoting differentiation, activation, and function in T cells, B cells, and antigen-presenting cells...
  8. pmc Fueling memories
    Jonathan D Powell
    Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Immunity 36:3-5. 2012
    ..In the current issue of Immunity, van der Windt et al. (2012) provide an important link between mitochondrial respiratory capacity and the development of CD8(+) T cell memory...
  9. pmc Anti-oxidant inhibition of hyaluronan fragment-induced inflammatory gene expression
    Michael Eberlein
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA
    J Inflamm (Lond) 5:20. 2008
    ..HA fragments, via a TLR and NF-kappaB pathway, induce inflammatory gene expression in macrophages and epithelial cells. NAC and DMSO are potent anti-oxidants which may help balance excess ROS states...
  10. ncbi request reprint Dissecting the mechanism of T-cell anergy with immunophilin ligands
    Jonathan D Powell
    Department of Oncology Immunology Hematopoiesis, Johns Hopkins School of Medicine, 1650 Orleans St, CRB 443, Baltimore, MD 21231, USA
    Curr Opin Investig Drugs 7:1002-7. 2006
    ..Finally, the clinical role of these compounds as immunosuppressive agents will be discussed in the context of their effects on promoting or inhibiting T-cell anergy...
  11. ncbi request reprint Threat matrix: low-molecular-weight hyaluronan (HA) as a danger signal
    Jonathan D Powell
    Bunting Blaustein Cancer Research Building, Johns Hopkins University School of Medicine, 1650 Orleans Street, Baltimore, MD 21231, USA
    Immunol Res 31:207-18. 2005
    ..In this review we hypothesize that low-molecular-weight species of the extracellular matrix polymer hyaluronan also performs this function by acting as an endogenous danger signal...
  12. ncbi request reprint The induction and maintenance of T cell anergy
    Jonathan D Powell
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, 1650 Orleans Street, Baltimore, MD 21231, USA
    Clin Immunol 120:239-46. 2006
    ....
  13. pmc HLA-haploidentical bone marrow transplantation for hematologic malignancies using nonmyeloablative conditioning and high-dose, posttransplantation cyclophosphamide
    Leo Luznik
    Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland, USA
    Biol Blood Marrow Transplant 14:641-50. 2008
    ..02). Nonmyeloablative HLA-haploidentical BMT with posttransplantation Cy is associated with acceptable rates of fatal graft failure and severe aGVHD or cGVHD...
  14. ncbi request reprint Rapamycin promotes emergence of IL-10-secreting donor lymphocyte infusion-derived T cells without compromising their graft-versus-leukemia reactivity
    Nadira Durakovic
    Division of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, USA
    Transplantation 83:631-40. 2007
    ..There are limited data examining the effects of pharmacological immunosuppression on the in vivo fate of donor lymphocyte infusions (DLI)-derived T cells, their function, and their antitumor efficacy...
  15. pmc High-dose cyclophosphamide as single-agent, short-course prophylaxis of graft-versus-host disease
    Leo Luznik
    Sidney Kimmel Comprehensive Cancer Center and Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Blood 115:3224-30. 2010
    ..These results suggest that high-dose posttransplantation cyclophosphamide is an effective single-agent prophylaxis of acute and chronic GVHD after BuCy conditioning and HLA-matched BMT (clinicaltrials.gov no. NCT00134017)...
  16. pmc Nonmyeloablative HLA-haploidentical bone marrow transplantation with high-dose posttransplantation cyclophosphamide: effect of HLA disparity on outcome
    Yvette L Kasamon
    Johns Hopkins University, 1650 Orleans Street, Baltimore, MD 21231, USA
    Biol Blood Marrow Transplant 16:482-9. 2010
    ..55, P = .03 for 3-4 vs fewer allele mismatches). Thus, greater HLA disparity does not appear to worsen overall outcome after NMA haploidentical BMT with high-dose posttransplantation cyclophosphamide...
  17. ncbi request reprint A role for mammalian target of rapamycin in regulating T cell activation versus anergy
    Yan Zheng
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University Medical Institutions, Baltimore, MD 21231, USA
    J Immunol 178:2163-70. 2007
    ..Overall, our data suggest that by integrating environmental cues, mTOR plays a central role in determining the outcome of Ag recognition...
  18. ncbi request reprint Low-dose radiation plus rapamycin promotes long-term bone marrow chimerism
    Jonathan D Powell
    Department of Oncology, Johns Hopkins School of Medicine, Baltimore, MD, USA
    Transplantation 80:1541-5. 2005
    ..Although a number of regimens have been explored, the optimal means of conditioning has not been determined...
  19. pmc NFAT binding and regulation of T cell activation by the cytoplasmic scaffolding Homer proteins
    Guo N Huang
    Program in Biochemistry, Cellular and Molecular Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Science 319:476-81. 2008
    ..These results demonstrate a further means by which costimulatory signals are regulated to control self-reactivity...
  20. pmc Factors governing the activation of adoptively transferred donor T cells infused after allogeneic bone marrow transplantation in the mouse
    Nadira Durakovic
    Divisions of Hematologic Malignancies, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, USA
    Blood 109:4564-74. 2007
    ....
  21. pmc Enhanced interaction between Hsp90 and raptor regulates mTOR signaling upon T cell activation
    Greg M Delgoffe
    Sidney Kimmel Comprehensive Cancer Research Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, United States
    Mol Immunol 46:2694-8. 2009
    ..Furthermore, full T cell activation during Hsp90 blockade leads to T cell tolerance in the form of anergy. Overall, our findings suggest that Hsp90 inhibitors might represent a novel means of promoting T cell tolerance...
  22. ncbi request reprint The novel cyclophilin binding compound, sanglifehrin A, disassociates G1 cell cycle arrest from tolerance induction
    Amy Allen
    Division of Immunology and Hematopoeisis, Department of Oncology, The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    J Immunol 172:4797-803. 2004
    ..Based on these data, we propose that the decision as to whether TCR engagement will lead to productive activation or tolerance is dictated by a rapamycin -inhibitable pathway, independent of the G(1)-->S phase cell cycle progression...
  23. pmc Genetic and biochemical regulation of CD4 T cell effector differentiation: insights from examination of T cell clonal anergy
    Christopher J Gamper
    Department of Oncology, Sidney Kimmel Cancer Center, School of Medicine, Johns Hopkins University, CRB 1, Room 443, Baltimore, MD 21231, USA
    Immunol Res 47:162-71. 2010
    ..We summarize our own findings and other recent advances in the genetic and biochemical understanding of T cell activation, tolerance, and plasticity in this review...
  24. ncbi request reprint Non-parametric, hypothesis-based analysis of microarrays for comparison of several phenotypes
    Jeanne Kowalski
    Department of Oncology, Johns Hopkins University, Baltimore, MD 21205, USA
    Bioinformatics 20:364-73. 2004
    ..The experiment was conducted to elucidate genes involved in pathways leading to T cell clonal anergy...
  25. pmc Cooperative B7-1/2 (CD80/CD86) and B7-DC costimulation of CD4+ T cells independent of the PD-1 receptor
    Tahiro Shin
    Sidneu Kimmel Comprehensive Cancer Centre, Johns Hopkins School of Medicine, Baltimore, MD 21231, USA
    J Exp Med 198:31-8. 2003
    ..Finally, costimulation with B7-DC alone or in conjunction with B7-1 is PD-1 independent, indicating that B7-DC costimulates T cells via a second receptor...
  26. pmc Anergic T cells are metabolically anergic
    Yan Zheng
    The Sidney Kimmel Cancer Research Center, The Johns Hopkins School of Medicine, Baltimore, MD 21231, USA
    J Immunol 183:6095-101. 2009
    ..Additionally, inhibition of these metabolic pathways during T cell activation leads to anergy in Th1-differentiated cells. Overall, our findings extend the role of T cell metabolism in regulating T cell function...
  27. pmc mTOR: taking cues from the immune microenvironment
    Greg M Delgoffe
    Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Immunology 127:459-65. 2009
    ..Specifically, we review the role of mTOR in promoting dendritic cell activation and maturation, in regulating full T cell activation versus anergy, and influencing the induction of regulatory T cells...
  28. ncbi request reprint NF-kappa B activation mediates the cross-talk between extracellular matrix and interferon-gamma (IFN-gamma) leading to enhanced monokine induced by IFN-gamma (MIG) expression in macrophages
    Maureen R Horton
    Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
    J Biol Chem 277:43757-62. 2002
    ..These data emphasize the ability of "degraded self" to activate/modify immune responses through the NF-kappaB pathway...
  29. ncbi request reprint Egr-2 and Egr-3 are negative regulators of T cell activation
    Meredith Safford
    The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Nat Immunol 6:472-80. 2005
    ..These data support the idea that Egr-2 and Egr-3 are involved in promoting a T cell receptor-induced negative regulatory genetic program...
  30. pmc Identification of DNA methyltransferase 3a as a T cell receptor-induced regulator of Th1 and Th2 differentiation
    Christopher J Gamper
    Department of Oncology, Johns Hopkins University, School of Medicine, Baltimore, MD 21231, USA
    J Immunol 183:2267-76. 2009
    ....
  31. ncbi request reprint Adenosine and anergy
    Paul E Zarek
    Department of Pharmacology and Molecular Sciences, Johns Hopkins School of Medicine, Baltimore, MD 21231, USA
    Autoimmunity 40:425-32. 2007
    ..Finally, we present evidence to suggest a possible role for adenosine A(2A) receptor signaling in T cell anergy...
  32. ncbi request reprint Hyaluronan fragments act as an endogenous danger signal by engaging TLR2
    Kara A Scheibner
    Division of Pulmonary and Critical Care Medicine, Department of Medicine, Johns Hopkins University School of Medicine, 1830 East Monument Street, Baltimore, MD 21205, USA
    J Immunol 177:1272-81. 2006
    ..Furthermore, we show that intact high m.w. HA can inhibit TLR-2 signaling. Finally, we demonstrate that LMW HA can act as an adjuvant promoting Ag-specific T cell responses in vivo in wild-type but not TLR-2(null) mice...
  33. ncbi request reprint Differential regulation of hyaluronan-induced IL-8 and IP-10 in airway epithelial cells
    Sada Boodoo
    Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Am J Physiol Lung Cell Mol Physiol 291:L479-86. 2006
    ..Furthermore, hyaluronan, by inducing IL-8 and IP-10 by distinct pathways, provides a unique target for differential regulation of key inflammatory chemokines...
  34. pmc The adenosine a2a receptor inhibits matrix-induced inflammation in a novel fashion
    Kara A Scheibner
    Department of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Am J Respir Cell Mol Biol 40:251-9. 2009
    ....

Research Grants2

  1. A2a receptor engagement promotes T cell tolerance
    Jonathan D Powell; Fiscal Year: 2010
    ..Understanding the role and mechanism by which the A2a receptor promotes T cell tolerance should provide insight in terms of devising specific clinical targets. ..
  2. INDUCTION AND MAINTENANCE OF T CELL ANERGY
    Jonathan Powell; Fiscal Year: 2002
    ....