James Pease is a Reader in Leukocyte Biology within the Inflammation, Repair and Development section of the National Heart and Lung Institute (NHLI) of Imperial College. He is also a principal investigator within the Medical Research Council/Asthma UK Centre in Allergic Mechanisms of Asthma and the British Heart Foundation Centre of Research Excellence.
James completed his BSc in Biochemistry at the University of Manchester before moving to the University of Sheffield where he studied for a PhD in the Department of Molecular Biology and Biotechnology. His PhD thesis concerned the characterization of the cell surface receptor for the complement fragment C5a and lead to a keen interest in the role of G protein-coupled receptors (GPCRs) involved in immunity. After completing a 4-year post-doctoral stint within the same department at the University of Sheffield, James moved to the laboratory of Dr Philip Murphy at the National Institutes of Health in Bethesda, Maryland, where he commenced studies on the recently discovered family of chemokine receptors. There he developed methodologies to examine the structure/function relationships of the receptors, identifying key domains of the proteins which were involved in binding both chemokine ligands and also HIV-1 envelope proteins.
James moved back to the UK in 1997 to the recently formed Leukocyte Biology Section within the NHLI at Imperial College London. There his interests included the identification of binding sites of prototypic small molecule antagonists of chemokine receptors with obvious therapeutic potential in a wide range of diseases. Current research interests of the group include other aspects of chemokine biology including regulation and trafficking of receptors, their role in disease and also the efforts of microbes to circumvent the chemokine system. Funding for the research comes from Arthritis UK, BBSRC, British Heart Foundation, MRC, Wellcome Trust and collaborations with pharmaceutical companies both in the UK and abroad.
James makes a significant contribution to undergraduate teaching within the Faculty of Medicine and was awarded his Certificate in Advanced Studies in Learning and Teaching (CASLAT) by the college in 2002. He is module lead for the Principles of Medicine (PoM) module which is the primary module in Phase Ia of the revised MBBS curriculum. James is also lead for module 3 of the BSc in Immunity and Infection within Phase II of the MBBS degree. He also sits on the editorial board of the publication Journal of Innate Immunity.
et al., 2019, Pulmonary environmental cues drive group 2 innate lymphoid cell dynamics in mice and humans, Science Immunology, Vol:4, ISSN:2470-9468
et al., 2019, A requirement for neutrophil glycosaminoglycans in chemokine:receptor interactions is revealed by the streptococcal protease SpyCEP, Journal of Immunology, Vol:202, ISSN:1550-6606, Pages:3246-3255
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, ISSN:0091-6749, Pages:552-553
Pontejo S, Murphy P, Pease JE, 2018, Chemokine subversion by human herpesviruses, Journal of Innate Immunity, Vol:10, ISSN:1662-811X, Pages:465-478
et al., 2018, Evidence for the existence of a CXCL17 receptor distinct from GPR35, Journal of Immunology, Vol:201, ISSN:0022-1767, Pages:714-724
et al., 2018, CXCL4/Platelet Factor 4 is an agonist of CCR1 and drives human monocyte migration, Scientific Reports, Vol:8, ISSN:2045-2322
et al., 2015, Pulmonary epithelial cell-derived cytokine TGF-β1 Is a critical cofactor for enhanced innate lymphoid cell function, Immunity, Vol:43, ISSN:1097-4180, Pages:945-958
et al., 2015, CXCR3 antagonist VUF10085 binds to an intrahelical site distinct from that of the broad spectrum antagonist TAK-779, British Journal of Pharmacology, Vol:172, ISSN:0007-1188, Pages:1822-1833
et al., 2014, Distinct Conformations of the Chemokine Receptor CCR4 with Implications for Its Targeting in Allergy, Journal of Immunology, Vol:192, ISSN:0022-1767, Pages:3419-3427
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, ISSN:0091-6749, Pages:150-157
et al., 2008, CXCL4-induced migration of activated T lymphocytes is mediated by the chemokine receptor CXCR3, Journal of Leukocyte Biology, Vol:83, ISSN:0741-5400, Pages:875-882
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
Pease JE, Williams TJ, 2006, Chemokines and their receptors in allergic disease, Journal of Allergy and Clinical Immunology, Vol:118, ISSN:0091-6749, Pages:305-318
et al., 2002, Regulation of CCR4 expression after segmental bronchial allergen challenge in atopic asthmatics, Journal of Allergy and Clinical Immunology, Vol:109, ISSN:0091-6749, Pages:S41-S41
et al., 2000, Delta 32 deletion of CCR5 gene and association with asthma or atopy, The Lancet, Vol:356, ISSN:0140-6736, Pages:1491-1492
et al., 2000, A small molecule antagonist of chemokine receptors CCR1 and CCR3 - Potent inhibition of eosinophil function and CCR3-mediated HIV-1 entry, Journal of Biological Chemistry, Vol:275, ISSN:0021-9258, Pages:25985-25992
et al., 1997, Identification of CCR8: A human monocyte and thymus receptor for the CC chemokine I-309, Journal of Experimental Medicine, Vol:186, ISSN:0022-1007, Pages:165-170