Publications
221 results found
Pease JE, Williams TJ, 2018, Tipping the balance: a biased nanobody antagonist of CCR3 with potential for the treatment of eosinophilic inflammation, Journal of Allergy and Clinical Immunology, Vol: 143, Pages: 552-553, ISSN: 0091-6749
Pease JE, Williams T, 2018, Eosinophils on trial, Clinical and Experimental Allergy, Vol: 48, Pages: 490-492, ISSN: 0954-7894
Williams TJ, 2015, Eotaxin-1 (CCL11), Frontiers in Immunology, Vol: 6, ISSN: 1664-3224
Finsterbusch M, Voisin M-B, Beyrau M, et al., 2014, Neutrophils recruited by chemoattractants in vivo induce microvascular plasma protein leakage through secretion of TNF, Journal of Experimental Medicine, Vol: 211, Pages: 1306-1313, ISSN: 1540-9538
Microvascular plasma protein leakage is an essential component of the inflammatoryresponse and serves an important function in local host defense and tissue repair. Mediatorssuch as histamine and bradykinin act directly on venules to increase the permeabilityof endothelial cell (EC) junctions. Neutrophil chemoattractants also induce leakage, aresponse that is dependent on neutrophil adhesion to ECs, but the underlying mechanismhas proved elusive. Through application of confocal intravital microscopy to the mousecremaster muscle, we show that neutrophils responding to chemoattractants release TNFwhen in close proximity of EC junctions. In vitro, neutrophils adherent to ICAM-1 or ICAM-2rapidly released TNF in response to LTB4, C5a, and KC. Further, in TNFR/ mice, neutrophilsaccumulated normally in response to chemoattractants administered to the cremastermuscle or dorsal skin, but neutrophil-dependent plasma protein leakage was abolished.Similar results were obtained in chimeric mice deficient in leukocyte TNF. A locally injectedTNF blocking antibody was also able to inhibit neutrophil-dependent plasma leakage, buthad no effect on the response induced by bradykinin. The results suggest that TNF mediatesneutrophil-dependent microvascular leakage. This mechanism may contribute to the effectsof TNF inhibitors in inflammatory diseases and indicates possible applications in lifethreateningacute edema.
Pease JE, Williams TJ, 2013, Editorial: Are all eotaxins created equal?, JOURNAL OF LEUKOCYTE BIOLOGY, Vol: 94, Pages: 207-209, ISSN: 0741-5400
- Author Web Link
- Cite
- Citations: 5
Rankin SM, Martin C, Burdon PC, et al., 2013, Bone marrow - birth place and grave yard for neutrophils, EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Vol: 43, Pages: 12-12, ISSN: 0014-2972
Williams TJ, 2012, New cell for asthma: enter the myeloid, THORAX, Vol: 67, Pages: 1114-1115, ISSN: 0040-6376
- Author Web Link
- Cite
- Citations: 1
Weller CL, Collington SJ, Williams T, et al., 2011, Mast cells in health and disease, CLINICAL SCIENCE, Vol: 120, Pages: 473-484, ISSN: 0143-5221
- Author Web Link
- Cite
- Citations: 67
Wise EL, Bonner KT, Williams TJ, et al., 2010, A single nucleotide polymorphism in the CCR3 gene ablates receptor export to the plasma membrane, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 126, Pages: 150-157, ISSN: 0091-6749
- Author Web Link
- Cite
- Citations: 9
Collington SJ, Hallgren J, Pease JE, et al., 2010, The Role of the CCL2/CCR2 Axis in Mouse Mast Cell Migration In Vitro and In Vivo, JOURNAL OF IMMUNOLOGY, Vol: 184, Pages: 6114-6123, ISSN: 0022-1767
- Author Web Link
- Cite
- Citations: 80
Collington SJ, Westwick J, Williams TJ, et al., 2010, The function of CCR3 on mouse bone marrow-derived mast cells <i>in vitro</i>, IMMUNOLOGY, Vol: 129, Pages: 115-124, ISSN: 0019-2805
- Author Web Link
- Cite
- Citations: 15
Williams TJ, Rankin SM, 2009, Chemokines and Phagocyte Trafficking, PHAGOCYTE-PATHOGEN INTERACTIONS: MACROPHAGES AND THE HOST RESPONSE TO INFECTION, Editors: Russell, Gordon, Publisher: AMER SOC MICROBIOLOGY, Pages: 93-106, ISBN: 978-1-55581-401-4
Pease JE, Williams TJ, 2009, Chemokines, Asthma and COPD, Editors: Barnes, Drazen, Rennard, Thomson, Publisher: Academic Press, ISBN: 9780123740014
The Second Edition of Asthma and COPD: Basic Mechanisms and Clinical Managementcontinues to provide a unique and authoritative comparison of asthma and COPD.
Pease JE, Williams TJ, 2008, Chemokines, Asthma and COPD: Basic Mechanisms and Clinical Management, Pages: 313-325, ISBN: 9780123740014
Chemokines have multiple roles in the organization of the immune system under basal conditions and during infection, and are also involved in angiogenesis. A crucial role of chemokines is the recruitment of different types of leukocytes from the blood to the sites of inflammation. Most of the known chemokines belong to two major families defined by the position of four conserved cysteine residues. The largest family is the CC chemokine family (28 in number), which possesses two adjacent cysteines in the vicinity of the N-terminus of the mature peptide. The CXC family (16 members) has two cysteine residues in this same region, but with an interposed amino acid. Chemokines are thought to bind to presenting molecules on the luminal surface of the venular endothelium, such as glycosaminoglycans, where the chemokines engage their receptors on the leukocyte surface. A combination of clinical observations, in vitro cell biology and in vivo animal modeling has delineated potentially important mechanisms underlying lung inflammation in COPD and asthma. These extensive studies support the hypothesis that chemokines have a fundamental role in regulating leukocyte trafficking in inflammatory disease. The chemokine receptors represent novel targets for treatment and therapeutic compounds have been described with efficacy in vitro and in vivo.
Meiser A, Mueller A, Wise EL, et al., 2008, The chemokine receptor CXCR3 is degraded following internalization and is replenished at the cell surface by de novo synthesis of receptor, JOURNAL OF IMMUNOLOGY, Vol: 180, Pages: 6713-6724, ISSN: 0022-1767
- Author Web Link
- Cite
- Citations: 99
Mueller A, Meiser A, McDonagh EM, et al., 2008, CXCL4-induced migration of activated T lymphocytes is mediated by the chemokine receptor CXCR3, JOURNAL OF LEUKOCYTE BIOLOGY, Vol: 83, Pages: 875-882, ISSN: 0741-5400
- Author Web Link
- Cite
- Citations: 80
Wise EL, Duchesnes C, da Fonseca PCA, et al., 2007, Small molecule receptor agonists and antagonists of CCR3 provide insight into mechanisms of chemokine receptor activation, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 282, Pages: 27935-27943
- Author Web Link
- Cite
- Citations: 51
Weller CL, Collington SJ, Hartnell A, et al., 2007, Chemotactic action of prostaglandin E2 on mouse mast cells acting via the PGE2 receptor 3, Proceedings of the National Academy of Sciences USA, Vol: 104, Pages: 11712-11717
Pease JE, Williams TJ, 2006, Chemokines and their receptors in allergic disease, JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, Vol: 118, Pages: 305-318, ISSN: 0091-6749
- Author Web Link
- Cite
- Citations: 77
Duchesnes UE, Murphy PM, Williams TJ, et al., 2006, Alanine scanning mutagenesis of the chemokine receptor CCR3 reveals distinct extracellular residues involved in recognition of the eotaxin family of chemokines, MOLECULAR IMMUNOLOGY, Vol: 43, Pages: 1221-1231, ISSN: 0161-5890
- Author Web Link
- Cite
- Citations: 25
Pease JE, Williams TJ, 2006, The attraction of chemokines as a target for specific anti-inflammatory therapy, BRITISH JOURNAL OF PHARMACOLOGY, Vol: 147, Pages: S212-S221, ISSN: 0007-1188
- Author Web Link
- Cite
- Citations: 62
Williams TJ, Weller CL, 2006, Population of lungs by mast cells., Novartis Found Symp, Vol: 279, Pages: 142-150, ISSN: 1528-2511
Mast cells are tissue-resident cells that are localized particularly in the skin, gastrointestinal tract and respiratory tract. They are mainly recognised for their role in adaptive immunity and allergy where cross-linking of surface-bound IgE results in acute mediator release giving early symptoms, and cytokine production contributing to chronic changes. The mast cell is now also increasingly recognized for its role in innate immunity conferred by its repertoire of complement and Toll receptors. Thus, mast cell deletion has been shown to suppress certain innate immune responses in murine models. Our interest is in the mechanisms involved in population of tissues by mast cells, particularly the airways. Mast cells are released from the bone marrow into the blood as committed precursors. These cells circulate in very low numbers and accumulate in tissues where they proliferate and mature under the influence of local cytokines and growth factors that define the mature phenotype appropriate for their location. Chemoattraction is important at critical phases in the life history of the mast cell, i.e. movement towards and through the bone marrow sinus endothelium, recruitment to tissues and movement within the tissues to the location of the mature cell. These phases are dependent on chemoattractants generated at specific locations acting on cell surface receptors whose repertoire evolves as the mast cell matures.
Weller CL, Collington SJ, Brown JK, et al., 2005, Leukotriene B-4, an activation product of mast cells, is a chemoattractant for their progenitors, Journal of Experimental Medicine, Vol: 201, Pages: 1961-1971, ISSN: 1540-9538
Mast cells are tissue-resident cells with important functions in allergy and inflammation. Pluripotential hematopoietic stem cells in the bone marrow give rise to committed mast cell progenitors that transit via the blood to tissues throughout the body, where they mature. Knowledge is limited about the factors that release mast cell progenitors from the bone marrow or recruit them to remote tissues. Mouse femoral bone marrow cells were cultured with IL-3 for 2 wk and a range of chemotactic agents were tested on the c-kit+ population. Cells were remarkably refractory and no chemotaxis was induced by any chemokines tested. However, supernatants from activated mature mast cells induced pronounced chemotaxis, with the active principle identified as leukotriene (LT) B4. Other activation products were inactive. LTB4 was highly chemotactic for 2-wk-old cells, but not mature cells, correlating with a loss of mRNA for the LTB4 receptor, BLT1. Immature cells also accumulated in vivo in response to intradermally injected LTB4. Furthermore, LTB4 was highly potent in attracting mast cell progenitors from freshly isolated bone marrow cell suspensions. Finally, LTB4 was a potent chemoattractant for human cord blood–derived immature, but not mature, mast cells. These results suggest an autocrine role for LTB4 in regulating tissue mast cell numbers.
Sabroe I, Jorritsma A, Stubbs VEL, et al., 2005, The carboxyl terminus of the chemokine receptor CCR3 contains distinct domains which regulate chemotactic signaling and receptor down-regulation in a ligand-dependent manner, EUROPEAN JOURNAL OF IMMUNOLOGY, Vol: 35, Pages: 1301-1310, ISSN: 0014-2980
- Author Web Link
- Cite
- Citations: 18
Weller CL, Jose PJ, Williams TJ, 2005, Selective suppression of leukocyte recruitment in allergic inflammation, MEMORIAS DO INSTITUTO OSWALDO CRUZ, Vol: 100, Pages: 153-160, ISSN: 0074-0276
- Author Web Link
- Cite
- Citations: 2
de Mendonça FL, da Fonseca PCA, Phillips RM, et al., 2005, Site-directed mutagenesis of CC chemokine receptor 1 reveals the mechanism of action of UCB 35625, a small molecule chemokine receptor antagonist, JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 280, Pages: 4808-4816
- Author Web Link
- Cite
- Citations: 65
Erin EM, Leaker BR, Zacharasiewicz AS, et al., 2005, Single dose topical coticosteroid inhibits IL-5 and IL-13 in nasal lavage following grass pollen challenge., Allergy, Vol: 60, Pages: 1524-1529
Erin EM, Zacharasiewicz AS, Nicholson GC, et al., 2005, Topical corticosteroid inhibits IL-4, IL-5 and IL-13 in nasal secretions following allergen challenge, Clinical and Experimental Allergy, Vol: 35, Pages: 1608-1614
Hartnell A, Heinemann A, Conroy DM, et al., 2004, Identification of selective basophil chemoattractants in human nasal polyps as insulin-like growth factor-1 and insulin-like growth factor-2, JOURNAL OF IMMUNOLOGY, Vol: 173, Pages: 6448-6457, ISSN: 0022-1767
- Author Web Link
- Cite
- Citations: 33
Medeiros AI, Malheiro A, Jose PJ, et al., 2004, Differential release of MIP-1α and eotaxin during infection of mice by <i>Histoplasma capsulatum</i> or inoculation of β-glucan, INFLAMMATION RESEARCH, Vol: 53, Pages: 351-354, ISSN: 1023-3830
- Author Web Link
- Cite
- Citations: 11
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.