Alasdair M Gilfillan

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Regulation of mast cell responses in health and disease
    Alasdair M Gilfillan
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    Crit Rev Immunol 31:475-529. 2011
  2. pmc Mast cell biology: introduction and overview
    Alasdair M Gilfillan
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Adv Exp Med Biol 716:2-12. 2011
  3. ncbi request reprint Integrated signalling pathways for mast-cell activation
    Alasdair M Gilfillan
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C206, 10 Center Drive, MSC 1881, Bethesda, Maryland 20892 1881, USA
    Nat Rev Immunol 6:218-30. 2006
  4. pmc A novel KIT-deficient mouse mast cell model for the examination of human KIT-mediated activation responses
    Daniel Smrz
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, MSC 1881, Bethesda, MD 20892 1881, USA
    J Immunol Methods 390:52-62. 2013
  5. pmc Kit- and Fc epsilonRI-induced differential phosphorylation of the transmembrane adaptor molecule NTAL/LAB/LAT2 allows flexibility in its scaffolding function in mast cells
    Shoko Iwaki
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, MSC 1881, Bethesda, MD 20892 1881, USA
    Cell Signal 20:195-205. 2008
  6. pmc The phosphoinositide 3-kinase-dependent activation of Btk is required for optimal eicosanoid production and generation of reactive oxygen species in antigen-stimulated mast cells
    Hye Sun Kuehn
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 181:7706-12. 2008
  7. pmc Synergistic activation of phospholipases Cgamma and Cbeta: a novel mechanism for PI3K-independent enhancement of FcepsilonRI-induced mast cell mediator release
    Hye Sun Kuehn
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892 1881, USA
    Cell Signal 20:625-36. 2008
  8. pmc Stem cell factor programs the mast cell activation phenotype
    Tomonobu Ito
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 188:5428-37. 2012
  9. ncbi request reprint Btk plays a crucial role in the amplification of Fc epsilonRI-mediated mast cell activation by kit
    Shoko Iwaki
    Laboratory of Allergic Diseases, NIAID, National Institutes of Health, Bethesda, Maryland 20892 1881, USA
    J Biol Chem 280:40261-70. 2005
  10. ncbi request reprint NTAL phosphorylation is a pivotal link between the signaling cascades leading to human mast cell degranulation following Kit activation and Fc epsilon RI aggregation
    Christine Tkaczyk
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Blood 104:207-14. 2004

Collaborators

Detail Information

Publications59

  1. pmc Regulation of mast cell responses in health and disease
    Alasdair M Gilfillan
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    Crit Rev Immunol 31:475-529. 2011
    ....
  2. pmc Mast cell biology: introduction and overview
    Alasdair M Gilfillan
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Adv Exp Med Biol 716:2-12. 2011
    ..This introductory chapter outlines and highlights the various topics of mast cell biology that will be discussed in further detail in subsequent chapters...
  3. ncbi request reprint Integrated signalling pathways for mast-cell activation
    Alasdair M Gilfillan
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C206, 10 Center Drive, MSC 1881, Bethesda, Maryland 20892 1881, USA
    Nat Rev Immunol 6:218-30. 2006
    ....
  4. pmc A novel KIT-deficient mouse mast cell model for the examination of human KIT-mediated activation responses
    Daniel Smrz
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, MSC 1881, Bethesda, MD 20892 1881, USA
    J Immunol Methods 390:52-62. 2013
    ..This cell line thus presents a novel system to delineate how MC function is modulated by native and mutated KIT and for the identification of novel inhibitors of these processes...
  5. pmc Kit- and Fc epsilonRI-induced differential phosphorylation of the transmembrane adaptor molecule NTAL/LAB/LAT2 allows flexibility in its scaffolding function in mast cells
    Shoko Iwaki
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, MSC 1881, Bethesda, MD 20892 1881, USA
    Cell Signal 20:195-205. 2008
    ..The observations reported herein support the conclusion that NTAL may be differentially utilized by specific receptors for relaying alternative signals and this suggests a flexibility in the function of TRAPs not previously appreciated...
  6. pmc The phosphoinositide 3-kinase-dependent activation of Btk is required for optimal eicosanoid production and generation of reactive oxygen species in antigen-stimulated mast cells
    Hye Sun Kuehn
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 181:7706-12. 2008
    ..These data demonstrate that strategies to decrease mast cell production of ROS and eicosanoids would have to target both ERK1/2- and PI3K/Btk-dependent pathways...
  7. pmc Synergistic activation of phospholipases Cgamma and Cbeta: a novel mechanism for PI3K-independent enhancement of FcepsilonRI-induced mast cell mediator release
    Hye Sun Kuehn
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892 1881, USA
    Cell Signal 20:625-36. 2008
    ..These responses were critical for the promotion of degranulation. This is the first report of synergistic activation between PLCgamma and PLCbeta that permits reinforcement of signals for degranulation in mast cells...
  8. pmc Stem cell factor programs the mast cell activation phenotype
    Tomonobu Ito
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 188:5428-37. 2012
    ....
  9. ncbi request reprint Btk plays a crucial role in the amplification of Fc epsilonRI-mediated mast cell activation by kit
    Shoko Iwaki
    Laboratory of Allergic Diseases, NIAID, National Institutes of Health, Bethesda, Maryland 20892 1881, USA
    J Biol Chem 280:40261-70. 2005
    ..These data demonstrate, for the first time, that Btk is a key regulator of a Kit-mediated amplification pathway that augments Fc epsilonRI-mediated mast cell activation...
  10. ncbi request reprint NTAL phosphorylation is a pivotal link between the signaling cascades leading to human mast cell degranulation following Kit activation and Fc epsilon RI aggregation
    Christine Tkaczyk
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Blood 104:207-14. 2004
    ..NTAL, thus, appears to be an important link between the signaling pathways that are initiated by these receptors, culminating in mast cell degranulation...
  11. pmc mTORC1 and mTORC2 differentially regulate homeostasis of neoplastic and non-neoplastic human mast cells
    Daniel Smrz
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    Blood 118:6803-13. 2011
    ....
  12. pmc Btk-dependent Rac activation and actin rearrangement following FcepsilonRI aggregation promotes enhanced chemotactic responses of mast cells
    Hye Sun Kuehn
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892 1881, USA
    J Cell Sci 123:2576-85. 2010
    ..Taken together, these data demonstrate that, by regulating signaling pathways that control F-actin rearrangement, Btk is crucial for the ability of antigen to amplify mast-cell chemotactic responses...
  13. pmc RGS13 controls g protein-coupled receptor-evoked responses of human mast cells
    Geetanjali Bansal
    Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 181:7882-90. 2008
    ..RGS13 overexpression inhibited CXCL12-evoked Ca(2+) mobilization, Akt phosphorylation and chemotaxis. These results suggest that RGS13 restricts certain GPCR-mediated biological responses of human mast cells...
  14. pmc Prostaglandin E2 activates and utilizes mTORC2 as a central signaling locus for the regulation of mast cell chemotaxis and mediator release
    Hye Sun Kuehn
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 286:391-402. 2011
    ..These findings are consistent with the conclusion that activation of mTORC2, downstream of PI3K, represents a critical signaling locus for chemotaxis and chemokine release from PGE(2)-activated mast cells...
  15. pmc CD72 negatively regulates KIT-mediated responses in human mast cells
    Tatsuki R Kataoka
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 184:2468-75. 2010
    ..Furthermore, BU40 and rCD100 also downregulated the growth of the HMC1.2 human mast cell line. Thus, targeting CD72 may provide a novel approach to the suppression of mast cell disease such as mastocytosis...
  16. ncbi request reprint Kit and FcepsilonRI mediate unique and convergent signals for release of inflammatory mediators from human mast cells
    Thomas R Hundley
    National Institutes of Health, Bethesda, MD 20892 1760, USA
    Blood 104:2410-7. 2004
    ..The findings, in total, indicated that a combination of FcepsilonRI and Kit-mediated signals and transcriptional processes were required for optimal physiologic responses of human mast cells to antigen...
  17. pmc Concurrent inhibition of kit- and FcepsilonRI-mediated signaling: coordinated suppression of mast cell activation
    Bettina M Jensen
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C206, 10 Center Drive, MSC 1881, Bethesda, MD 20892 1881, USA
    J Pharmacol Exp Ther 324:128-38. 2008
    ....
  18. pmc Activation and function of the mTORC1 pathway in mast cells
    Mi Sun Kim
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA
    J Immunol 180:4586-95. 2008
    ..Specifically, the mTORC1 pathway may play a critical role in normal and dysregulated control of mast cell homeostasis...
  19. ncbi request reprint Cutting edge: genetic variation influences Fc epsilonRI-induced mast cell activation and allergic responses
    Yumi Yamashita
    Molecular Inflammation Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 179:740-3. 2007
    ..The findings demonstrate a genetic influence on the extent of a mast cell's response and identify Fyn kinase as a contributory determinant...
  20. pmc A truncated splice-variant of the FcεRIβ receptor subunit is critical for microtubule formation and degranulation in mast cells
    Glenn Cruse
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Immunity 38:906-17. 2013
    ..Because t-FcεRIβ has this critical function, it represents a therapeutic target for the downregulation of allergic inflammation...
  21. pmc IL-33 induces a hyporesponsive phenotype in human and mouse mast cells
    Mi Yeon Jung
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 190:531-8. 2013
    ..The ability to downregulate MC activation in this manner may provide alternative approaches for treatment of MC-driven disease...
  22. pmc Glycogen synthase kinase-3β is a prosurvival signal for the maintenance of human mast cell homeostasis
    Madeleine Radinger
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    J Immunol 187:5587-95. 2011
    ..Our data suggest that targeting of GSK3β with small m.w. inhibitors such as CHIR 99021 may thus provide a mechanism for limiting mast cell survival and subsequently decreasing the intensity of the allergic inflammatory response...
  23. ncbi request reprint The phospholipase C gamma 1-dependent pathway of Fc epsilon RI-mediated mast cell activation is regulated independently of phosphatidylinositol 3-kinase
    Christine Tkaczyk
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 278:48474-84. 2003
    ..However, PI 3-kinase may contribute to the later phase of Fc epsilon RI-mediated degranulation in human mast cells...
  24. ncbi request reprint Cutting Edge: Lentiviral short hairpin RNA silencing of PTEN in human mast cells reveals constitutive signals that promote cytokine secretion and cell survival
    Yasuko Furumoto
    Molecular Inflammation Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 176:5167-71. 2006
    ..The findings demonstrate that PTEN functions as a key regulator of mast cell homeostasis and FcepsilonRI-responsiveness...
  25. pmc Mechanisms of mast cell signaling in anaphylaxis
    Dean D Metcalfe
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
    J Allergy Clin Immunol 124:639-46; quiz 647-8. 2009
    ..These studies have revealed that signaling pathways exist to both upregulate and downregulate mast cell responses. In this review we will thus describe the key molecular players in these pathways in the context of anaphylaxis...
  26. pmc Knockout of the Trpc1 gene reveals that TRPC1 can promote recovery from anaphylaxis by negatively regulating mast cell TNF-α production
    Nevenka Medic
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892 1881, USA
    Cell Calcium 53:315-26. 2013
    ..These data thus provide evidence that, in this model, TRPC1 promotes recovery from the anaphylactic response by repressing antigen-mediated TNF-α release from MCs...
  27. pmc Prevention of F-actin assembly switches the response to SCF from chemotaxis to degranulation in human mast cells
    Daniel Smrz
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
    Eur J Immunol 43:1873-82. 2013
    ..These observations suggest that processes regulating cell migration limit MC degranulation as a consequence of cytoskeletal reorganization. ..
  28. pmc KIT GNNK splice variants: expression in systemic mastocytosis and influence on the activating potential of the D816V mutation in mast cells
    Eunice Ching Chan
    Mast Cell Biology Section, Laboratory of Allergic Diseases, Bethesda, MD, USA
    Exp Hematol 41:870-881.e2. 2013
    ..These data suggest that neoplastic mast cells favor a GNNK(-) variant predominance, which in turn enhances the activating potential of the KIT D816V mutation and thus could influence therapeutic sensitivity in systemic mastocytosis. ..
  29. pmc Distinct PGE2-responder and non-responder phenotypes in human mast cell populations: "all or nothing" enhancement of antigen-dependent mediator release
    Hye Sun Kuehn
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    Immunol Lett 141:45-54. 2011
    ..However, translocation of PLCγ(1) to the cell membrane and the associated calcium signal were enhanced only in the responder HuMC population indicating that the link between EP3 and PLCγ is impaired in the non-responder HuMCs...
  30. pmc Glycogen synthase kinase 3beta activation is a prerequisite signal for cytokine production and chemotaxis in human mast cells
    Madeleine Radinger
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    J Immunol 184:564-72. 2010
    ..These studies provide evidence for a novel prerequisite priming mechanism for KIT-dependent responses regulated by GSK3beta in HuMCs...
  31. ncbi request reprint Comparison of Fc epsilon RI- and Fc gamma RI-mediated degranulation and TNF-alpha synthesis in human mast cells: selective utilization of phosphatidylinositol-3-kinase for Fc gamma RI-induced degranulation
    Yoshimichi Okayama
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C206, 10 Center Drive MSC 1881, Bethesda, MD 20892 1881, USA
    Eur J Immunol 33:1450-9. 2003
    ..The one exception was that, although phosphatidylinositol-3-kinase was activated after both Fc epsilon RI and Fc gamma RI aggregation, only the Fc gamma RI appeared to require this molecule for degranulation...
  32. pmc Canonical transient receptor potential 5 channel in conjunction with Orai1 and STIM1 allows Sr2+ entry, optimal influx of Ca2+, and degranulation in a rat mast cell line
    Hong Tao Ma
    Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 180:2233-9. 2008
    ..These and other observations suggest that the Sr(2+)-permeable TRPC5 associates with STIM1 and Orai1 in a stoichiometric manner to enhance entry of Ca(2+) to generate a signal for degranulation...
  33. pmc Amplification mechanisms for the enhancement of antigen-mediated mast cell activation
    Alasdair M Gilfillan
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD, 20892 1881, USA
    Immunol Res 43:15-24. 2009
    ..In this review, we describe our research exploring the mechanisms regulating these synergistic interactions and, furthermore, discuss the relevance of our observations in the context of clinical considerations...
  34. pmc The multiple roles of phosphoinositide 3-kinase in mast cell biology
    Mi Sun Kim
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Trends Immunol 29:493-501. 2008
    ..Furthermore, we describe how different mast cell receptors use alternative isoforms of PI3K for these functions and discuss potential downstream targets of these isoforms...
  35. ncbi request reprint Roles of adaptor molecules in mast cell activation
    Shoko Iwaki
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    Chem Immunol Allergy 87:43-58. 2005
    ..In this chapter, we discuss the structure and properties of these molecules and how these proteins regulate the cellular processes associated with receptor-mediated mast cell activation...
  36. pmc TLR-mediated signaling pathways circumvent the requirement for DAP12 in mast cells for the induction of inflammatory mediator release
    Daniel Smrz
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    Eur J Immunol 40:3557-69. 2010
    ....
  37. pmc Endosomal trafficking of the ligated FcvarepsilonRI receptor
    Gul nar V Fattakhova
    Receptor Cell Biology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, United States
    Mol Immunol 46:793-802. 2009
    ....
  38. ncbi request reprint Identification of Fyn-binding proteins in MC/9 mast cells using mass spectrometry
    Dong Ho Nahm
    National Institutes of Health, National Institute of Allergy and Infectious Diseases, Laboratory of Allergic Diseases, Building 10, Room 11C206, 10 Center Drive, Bethesda, MD 20892 1881, USA
    Biochem Biophys Res Commun 310:202-8. 2003
    ....
  39. ncbi request reprint 5-hydroxytryptamine induces mast cell adhesion and migration
    Nataliya M Kushnir-Sukhov
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA
    J Immunol 177:6422-32. 2006
    ..Furthermore, both mouse and human MC respond to 5-HT through the 5-HT(1A) receptor. Our data are consistent with the conclusion that 5-HT promotes inflammation by increasing MC at the site of tissue injury...
  40. pmc Diminished allergic disease in patients with STAT3 mutations reveals a role for STAT3 signaling in mast cell degranulation
    Andrea M Siegel
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD
    J Allergy Clin Immunol 132:1388-96. 2013
    ....
  41. pmc G protein-coupled receptors and the modification of FcepsilonRI-mediated mast cell activation
    Hye Sun Kuehn
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892 1881, USA
    Immunol Lett 113:59-69. 2007
    ..Furthermore, we discuss the potential mechanisms whereby the signalling responses utilized by the FcepsilonRI for mast cell activation are influenced by those initiated by GPCRs to produce these diverse responses...
  42. pmc Generation, isolation, and maintenance of human mast cells and mast cell lines derived from peripheral blood or cord blood
    Madeleine Radinger
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Curr Protoc Immunol . 2010
    ..In this unit, techniques for the development and culture of human mast cells from their progenitors and the culture of human mast cell lines are described. The relative merits and drawbacks of each model are also described...
  43. pmc Measuring mast cell mediator release
    Hye Sun Kuehn
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    Curr Protoc Immunol . 2010
    ....
  44. pmc Ntal/Lab/Lat2
    Shoko Iwaki
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C206, 10 Center Drive, MSC 1881, Bethesda, MD 20892 1881, USA
    Int J Biochem Cell Biol 39:868-73. 2007
    ....
  45. ncbi request reprint Fcgamma receptors on mast cells: activatory and inhibitory regulation of mediator release
    Christine Tkaczyk
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    Int Arch Allergy Immunol 133:305-15. 2004
    ..The exploitation of FcgammaRs for a potential therapy for the treatment of allergic disorders is discussed in this context...
  46. pmc Examination of the role of TRPM8 in human mast cell activation and its relevance to the etiology of cold-induced urticaria
    Nevenka Medic
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1881, USA
    Cell Calcium 50:473-80. 2011
    ..From these data, we conclude that TRPM8 is unlikely to directly regulate mast cell activation in cold urticaria. Thus, alternative mechanisms likely exist for the pathogenesis of this disease...
  47. ncbi request reprint Targeting kit activation: a potential therapeutic approach in the treatment of allergic inflammation
    Bettina M Jensen
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C206, 10 Center Drive MSC 1881, Bethesda, MD 20892 1881, USA
    Inflamm Allergy Drug Targets 6:57-62. 2007
    ..In this review, we provide an overview of the role of SCF and Kit in mast cell activation and discuss potential drug candidates for targeting this response...
  48. doi request reprint Generation, isolation, and maintenance of rodent mast cells and mast cell lines
    Bettina M Jensen
    National Institutes of Health, Bethesda, Maryland, USA
    Curr Protoc Immunol . 2006
    ..In this unit, we describe the protocols used for the isolation and/or culture of these cells and discuss the relative merits of their use...
  49. ncbi request reprint IgE-dependent activation of sphingosine kinases 1 and 2 and secretion of sphingosine 1-phosphate requires Fyn kinase and contributes to mast cell responses
    Ana Olivera
    Molecular Inflammation Section, Molecular Immunology and Inflammation Branch, NIAMS, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 281:2515-25. 2006
    ..Taken together with our previous study, which demonstrated delayed SphK activation in Lyn-deficient BMMC, we propose a cooperative role between Fyn and Lyn kinases in the activation of SphKs, which contributes to mast cell responses...
  50. ncbi request reprint The high-affinity immunoglobulin-E receptor (FcepsilonRI) is endocytosed by an AP-2/clathrin-independent, dynamin-dependent mechanism
    Gul nar Fattakhova
    Receptor Cell Biology Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA
    Traffic 7:673-85. 2006
    ..We conclude that internalization of cross-linked FcRI does not require the AP-2/clathrin complex but is dynamin-dependent and may be lipid raft mediated...
  51. ncbi request reprint Determination of protein phosphorylation in Fc epsilon RI-activated human mast cells by immunoblot analysis requires protein extraction under denaturing conditions
    Christine Tkaczyk
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C213, 10 Center Drive MSC 1881, Bethesda, MD 20892 1881, USA
    J Immunol Methods 268:239-43. 2002
    ..The data presented in this report would be applicable to other cell types where high concentrations of proteases are present...
  52. ncbi request reprint Activation of human mast cells through the high affinity IgG receptor
    Christine Tkaczyk
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C205, 10 Center Drive MSC 1881, Bethesda, MD 2089 1881, USA
    Mol Immunol 38:1289-93. 2002
    ..These observations provide evidence that human mast cells may also be recruited into inflammation through IgG-dependent mechanisms...
  53. pmc IgE-FcepsilonRI interactions determine HIV coreceptor usage and susceptibility to infection during ontogeny of mast cells
    J Bruce Sundstrom
    Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA
    J Immunol 182:6401-9. 2009
    ....
  54. pmc Defective eosinophil hematopoiesis ex vivo in inbred Rocky Mountain White (IRW) mice
    Kimberly D Dyer
    Eosinophil Biology Section, Laboratory of Allergic Diseases, National Institute of Allergy andInfectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    J Leukoc Biol 90:1101-9. 2011
    ..These results suggest that IRW mice have diminished capacity to generate eosinophils in culture and in vivo, likely as a result of diminished signaling via IL-5Rα...
  55. pmc The tyrosine kinase network regulating mast cell activation
    Alasdair M Gilfillan
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 1930, USA
    Immunol Rev 228:149-69. 2009
    ..In this review, we discuss the regulation and role of specific members of this tyrosine kinase network in KIT and Fc epsilon RI-mediated mast cell activation...
  56. ncbi request reprint Molecular regulation of mast cell activation
    Juan Rivera
    Molecular Inflammation Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892 1820, USA
    J Allergy Clin Immunol 117:1214-25; quiz 1226. 2006
    ..The unifying theme is that the regulatory steps mentioned herein are required for promoting effective responses while protecting against unwanted inflammatory responses...
  57. ncbi request reprint Adaptive and innate immune reactions regulating mast cell activation: from receptor-mediated signaling to responses
    Christine Tkaczyk
    Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C206, 10 Center Drive, MSC 1881, Bethesda, MD 20892, USA
    Immunol Allergy Clin North Am 26:427-50. 2006
    ..The exact interconnections between the signaling pathways initiated by the surface receptors described in this article remain to be completely worked out; thus, this remains a topic for future investigation...
  58. ncbi request reprint Nitric oxide inhibits IgE-dependent cytokine production and Fos and Jun activation in mast cells
    Beverley J Davis
    Department of, Pharmacology, University of Liverpool, United Kingdom
    J Immunol 173:6914-20. 2004
    ..These results show that NO is capable of inhibiting FcepsilonRI-dependent mast cell cytokine production at the level of gene regulation, and suggest too that NO may contribute to resolution of allergic inflammation...
  59. ncbi request reprint Essential role for the p110delta phosphoinositide 3-kinase in the allergic response
    Khaled Ali
    Ludwig Institute for Cancer Research, 91 Riding House Street, London W1W 7BS, UK
    Nature 431:1007-11. 2004
    ..Inactivation of p110delta protects mice against anaphylactic allergic responses. These results identify p110delta as a new target for therapeutic intervention in allergy and mast-cell-related pathologies...