Regulation of Chemokine- Receptor Interactions and Functions

International Journal of Molecular Sciences Regulation of Chemokine- Books Receptor Interactions and Functions Edited by Martin J. Stone Printed Edition of the Special Issue Published in IJMS www.mdpi.com/journal/ijms MDPI Regulation of Chemokine-Receptor Interactions and Functions Special Issue Editor Martin J. Stone Books MDPI • Basel • Beijing • Wuhan • Barcelona • Belgrade MDPI Special Issue Editor Martin J. Stone Monash University Australia Editorial Office MDPI AG St. Alban-Anlage 66 Basel, Switzerland This edition is a reprint of the Special Issue published online in the open access journal International Journal of Molecular Sciences (ISSN 1422-0067) in 2017 (available at: http://www.mdpi.com/journal/ijms/special_issues/chemokine_receptor_2016). For citation purposes, cite each article independently as indicated on the article Books page online and as indicated below: Lastname, F.M.; Lastname, F.M. Article title. Journal Name. Year. Article number, page range. First Edition 2018 ISBN 978-3-03842-728-5 (Pbk) ISBN 978-3-03842-727-8 (PDF) Cover image: Neutrophil chemotaxis in mouse postcapillary venules, visualised by intravital imaging. Cover photo courtesy of Professor Michael Hickey, Monash University, VIC, Australia. Articles in this volume are Open Access and distributed under the Creative Commons Attribution license (CC BY), which allows users to download, copy and build upon published articles even for commercial purposes, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. The book taken as a whole is © 2018 MDPI, Basel, Switzerland, distributed under the terms and conditions of the Creative Commons license CC BY-NC-ND (http://creativecommons.org/licenses/by-nc-nd/4.0/). MDPI Table of Contents About the Special Issue Editor ...................................... v Martin J. Stone Regulation of Chemokine–Receptor Interactions and Functions doi: 10.3390/ijms18112415 ....................................... 1 Martin J. Stone, Jenni A. Hayward, Cheng Huang, Zil E. Huma and Julie Sanchez Mechanisms of Regulation of the Chemokine-Receptor Network doi: 10.3390/ijms18020342 ....................................... 6 Michelle C. Miller and Kevin H. Mayo Chemokines from a Structural Perspective doi: 10.3390/ijms18102088 ....................................... 39 Sarah Thompson, Beatriz Martnez-Burgo, Krishna Mohan Sepuru, Krishna Rajarathnam, John A. Kirby, Neil S. Sheerin and Simi Ali Regulation of Chemokine Function: The Roles of GAG-Binding and Post-Translational Nitration doi: 10.3390/ijms18081692 ....................................... 55 Aaron J. Brown, Krishna Mohan Sepuru and Krishna Rajarathnam Structural Basis of Native CXCL7 Monomer Binding to CXCR2 Receptor N-Domain and Glycosaminoglycan Heparin Books doi: 10.3390/ijms18030508 ....................................... 72 Aaron J. Brown, Prem Raj B. Joseph, Kirti V. Sawant and Krishna Rajarathnam Chemokine CXCL7 Heterodimers: Structural Insights, CXCR2 Receptor Function, and Glycosaminoglycan Interactions doi: 10.3390/ijms18040748 ....................................... 88 Mieke Metzemaekers, Anneleen Mortier, Rik Janssens, Daiane Boff, Lotte Vanbrabant, Nicole Lamoen, Jo Van Damme, Mauro M. Teixeira, Ingrid De Meester, Flvio A. Amaral and Paul Proost Glycosaminoglycans Regulate CXCR3 Ligands at Distinct Levels: Protection against Processing by Dipeptidyl Peptidase IV/CD26 and Interference with Receptor Signaling doi: 10.3390/ijms18071513 .......................................106 Anna F. Nguyen, Megan S. Schill, Mike Jian and Patricia J. LiWang The Effect of N-Terminal Cyclization on the Function of the HIV Entry Inhibitor 5P12-RANTES doi: 10.3390/ijms18071575 .......................................130 Natasha A. Moussouras, Anthony E. Getschman, Emily R. Lackner, Christopher T. Veldkamp, Michael B. Dwinell and Brian F. Volkman Differences in Sulfotyrosine Binding amongst CXCR1 and CXCR2 Chemokine Ligands doi: 10.3390/ijms18091894 .......................................145 Andrew J. Phillips, Deni Taleski, Chad A. Koplinski, Anthony E. Getschman, Natasha A. Moussouras, Amanda M. Richard, Francis C. Peterson, Michael B. Dwinell, Brian F. Volkman, Richard J. Payne and Christopher T. Veldkamp CCR7 Sulfotyrosine Enhances CCL21 Binding doi: 10.3390/ijms18091857 .......................................160 iii MDPI Vivian Adamski, Rolf Mentlein, Ralph Lucius, Michael Synowitz, Janka Held-Feindt and Kirsten Hattermann The Chemokine Receptor CXCR6 Evokes Reverse Signaling via the Transmembrane Chemokine CXCL16 doi: 10.3390/ijms18071468 .......................................173 Anna F. Nguyen, Nai-Wei Kuo, Laura J. Showalter, Ricardo Ramos, Cynthia M. Dupureur, Michael E. Colvin and Patricia J. LiWang Biophysical and Computational Studies of the vCCI:vMIP-II Complex doi: 10.3390/ijms18081778 .......................................187 Ryosuke Sakumoto, Ken-Go Hayashi, Shiori Fujii, Hiroko Kanahara, Misa Hosoe, Tadashi Furusawa and Keiichiro Kizaki Possible Roles of CC- and CXC-Chemokines in Regulating Bovine Endometrial Function during Early Pregnancy doi: 10.3390/ijms18040742 .......................................205 Books iv MDPI About the Special Issue Editor Martin J. Stone is a researcher and teacher in the Monash University Department of Biochemistry and Molecular Biology and the Monash Biomedicine Discovery Institute, Melbourne, Australia. He received his BSc and MSc(Hons) degrees from the University of Auckland (New Zealand) and his PhD from the University of Cambridge (UK). He was a postdoctoral research fellow at the Scripps Research Institute in (San Diego, USA) and a faculty member at Indiana University (Bloomington, USA) before moving to Monash in 2007. Associate Professor Stone’s research focuses on the biochemistry and pharmacology of chemokines and their receptors, which are critical in directing migration of leukocytes in inflammatory responses. Recently, his lab has made important contributions to under- standing the influence of receptor tyrosine sulfation on chemokine recognition, the structural basis by which chemokines differentially activate a shared receptor, and the discovery of tick proteins that suppress chemokine-mediated host defenses. Books v MDPI MDPI Books International Journal of Molecular Sciences Editorial Regulation of Chemokine–Receptor Interactions and Functions Martin J. Stone Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Clayton VIC 3800, Australia; [email protected]; Tel.: +61-3-9902-9246 Received: 6 November 2017; Accepted: 10 November 2017; Published: 14 November 2017 Inflammation is the body’s response to injury or infection. As early as 2000 years ago, the Roman encyclopaedist Aulus Cornelius Celsus recognised four cardinal signs of this response—redness, heat, swelling and pain; a fifth sign is loss of function. The underlying cause of these common symptoms remained a mystery until the 19th century, when Rudolf Virchow “claim(ed) for the leukocyte a place in the field of pathology” [1]. It is now widely recognised that all inflammatory responses involve migration of leukocytes (white blood cells) to the affected tissues, where they accumulate and carry out a plethora of functions including elimination of pathogens, regulation of immunity and tissue repair. While leukocyte recruitment is a beneficial response to pathogen invasion, we are all too familiar Books with the detrimental roles it can play in numerous diseases. As an example, in allergic asthma, the recruited leukocytes include eosinophils, which can then undergo degranulation, releasing toxic proteins that induce airway constriction and difficulty breathing [2]. In this case, the inflammatory response causes more damage than the initial stimulus (the allergen), so it would be beneficial to suppress the leukocyte recruitment. The same is true in many other inflammatory diseases, such as atherosclerosis, rheumatoid arthritis, multiple sclerosis, dermatitis, etc. However, it is essential that such a therapeutic strategy should not suppress inflammation so much as to make the patient susceptible to infections. To successfully achieve the right balance between the “yin and yang” of inflammation, we need to understand the biochemical mechanisms underlying leukocyte recruitment. Enter chemokines and chemokine receptors. Over a period of about 20 years beginning in the late 1980s, researchers discovered a family of related proteins that are secreted by various cell types as an early response to tissue damage and attract leukocytes towards the affected tissues. These proteins were named chemokines (chemotactic cytokines) due to their ability to induce chemotaxis, which is migration of cells towards a chemical stimulus. They elicit this function by activating chemokine receptors, a family of G protein-coupled receptors expressed on the surfaces of leukocytes. Importantly, different types of leukocytes express different chemokine receptors, so much of the selectivity of leukocyte responses, i.e., which types of leukocytes are recruited in a given situation, arises from the complementarity between the specific chemokines expressed in the affected tissues and the specific receptors expressed on the different leukocytes. The chemokine–receptor network was clearly an attractive target to suppress unwanted inflammation while still enabling appropriate responses to pathogens. Following the discovery of chemokines

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