Exploring Chemokine Signaling LUNARIS™ Chemokine Kits
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C-X-C Motif Chemokine Ligand 10 Produced by Mouse Sertoli Cells in Response to Mumps Virus Infection Induces Male Germ Cell Apoptosis
Citation: Cell Death and Disease (2017) 8, e3146; doi:10.1038/cddis.2017.560 OPEN Macmillan Publishers Limited, part of Springer Nature. www.nature.com/cddis Corrected: Correction C-X-C motif chemokine ligand 10 produced by mouse Sertoli cells in response to mumps virus infection induces male germ cell apoptosis Qian Jiang1, Fei Wang1, Lili Shi1, Xiang Zhao1, Maolei Gong1, Weihua Liu1, Chengyi Song2, Qihan Li3, Yongmei Chen1, Han Wu*,1,2 and Daishu Han*,1 Mumps virus (MuV) infection usually results in germ cell degeneration in the testis, which is an etiological factor for male infertility. However, the mechanisms by which MuV infection damages male germ cells remain unclear. The present study showed that C-X-C motif chemokine ligand 10 (CXCL10) is produced by mouse Sertoli cells in response to MuV infection, which induces germ cell apoptosis through the activation of caspase-3. CXC chemokine receptor 3 (CXCR3), a functional receptor of CXCL10, is constitutively expressed in male germ cells. Neutralizing antibodies against CXCR3 and an inhibitor of caspase-3 activation significantly inhibited CXCL10-induced male germ cell apoptosis. Furthermore, the tumor necrosis factor-α (TNF-α) upregulated CXCL10 production in Sertoli cells after MuV infection. The knockout of either CXCL10 or TNF-α reduced germ cell apoptosis in the co-cultures of germ cells and Sertoli cells in response to MuV infection. Local injection of MuV into the testes of mice confirmed the involvement of CXCL10 in germ cell apoptosis in vivo. These results provide novel insights into MuV-induced germ cell apoptosis in the testis. -
Differentiation and Bone Resorption Role of CX3CL1/Fractalkine In
Role of CX3CL1/Fractalkine in Osteoclast Differentiation and Bone Resorption Keiichi Koizumi, Yurika Saitoh, Takayuki Minami, Nobuhiro Takeno, Koichi Tsuneyama, Tatsuro Miyahara, This information is current as Takashi Nakayama, Hiroaki Sakurai, Yasuo Takano, Miyuki of September 29, 2021. Nishimura, Toshio Imai, Osamu Yoshie and Ikuo Saiki J Immunol published online 18 November 2009 http://www.jimmunol.org/content/early/2009/11/18/jimmuno l.0803627.citation Downloaded from Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 29, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published November 18, 2009, doi:10.4049/jimmunol.0803627 The Journal of Immunology Role of CX3CL1/Fractalkine in Osteoclast Differentiation and Bone Resorption1 Keiichi Koizumi,2* Yurika Saitoh,* Takayuki Minami,* Nobuhiro Takeno,* Koichi Tsuneyama,†‡ Tatsuro Miyahara,§ Takashi Nakayama,¶ Hiroaki Sakurai,*† Yasuo Takano,‡ Miyuki Nishimura,ʈ Toshio Imai,ʈ Osamu Yoshie,¶ and Ikuo Saiki*† The recruitment of osteoclast precursors toward osteoblasts and subsequent cell-cell interactions are critical for osteoclast dif- ferentiation. -
S41467-017-02610-0.Pdf
ARTICLE DOI: 10.1038/s41467-017-02610-0 OPEN Angiogenic factor-driven inflammation promotes extravasation of human proangiogenic monocytes to tumours Adama Sidibe 1,4, Patricia Ropraz1, Stéphane Jemelin1, Yalin Emre 1, Marine Poittevin1, Marc Pocard2,3, Paul F. Bradfield1 & Beat A. Imhof1 1234567890():,; Recruitment of circulating monocytes is critical for tumour angiogenesis. However, how human monocyte subpopulations extravasate to tumours is unclear. Here we show mechanisms of extravasation of human CD14dimCD16+ patrolling and CD14+CD16+ inter- mediate proangiogenic monocytes (HPMo), using human tumour xenograft models and live imaging of transmigration. IFNγ promotes an increase of the chemokine CX3CL1 on vessel lumen, imposing continuous crawling to HPMo and making these monocytes insensitive to chemokines required for their extravasation. Expression of the angiogenic factor VEGF and the inflammatory cytokine TNF by tumour cells enables HPMo extravasation by inducing GATA3-mediated repression of CX3CL1 expression. Recruited HPMo boosts angiogenesis by secreting MMP9 leading to release of matrix-bound VEGF-A, which amplifies the entry of more HPMo into tumours. Uncovering the extravasation cascade of HPMo sets the stage for future tumour therapies. 1 Department of Pathology and Immunology, Centre Médical Universitaire (CMU), Medical faculty, University of Geneva, Rue Michel-Servet 1, CH-1211 Geneva, Switzerland. 2 Department of Oncologic and Digestive Surgery, AP-HP, Hospital Lariboisière, 2 rue Ambroise Paré, F-75475 Paris cedex 10, France. 3 Université Paris Diderot, Sorbonne Paris Cité, CART, INSERM U965, 49 boulevard de la Chapelle, F-75475 Paris cedex 10, France. 4Present address: Department of Physiology and Metabolism, Centre Médical Universitaire (CMU), Medical faculty, University of Geneva, Rue Michel-Servet 1, CH-1211 Geneva, Switzerland. -
CX3CR1 Deficiency Attenuates DNFB-Induced Contact
International Journal of Molecular Sciences Article CX3CR1 Deficiency Attenuates DNFB-Induced Contact Hypersensitivity through Skewed Polarization towards M2 Phenotype in Macrophages 1, 1, 1,2, 1,3 Sayaka Otobe y, Teruyoshi Hisamoto y, Tomomitsu Miyagaki * , Sohshi Morimura , Hiraku Suga 1, Makoto Sugaya 1,3 and Shinichi Sato 1 1 Department of Dermatology, the University of Tokyo Graduate School of Medicine, Tokyo 113-8655, Japan; confi[email protected] (S.O.); [email protected] (T.H.); [email protected] (S.M.); [email protected] (H.S.); [email protected] (M.S.); [email protected] (S.S.) 2 Department of Dermatology, St. Marianna University School of Medicine, Kanagawa 216-8511, Japan 3 Department of Dermatology, International University of Health and Welfare, Chiba 286-0124, Japan * Correspondence: [email protected]; Tel.: +81-44-977-8111; Fax: +81-44-977-3540 These authors contributed equally to this work. y Received: 28 September 2020; Accepted: 5 October 2020; Published: 7 October 2020 Abstract: CX3CL1 can function as both an adhesion molecule and a chemokine for CX3CR1+ cells, such as T cells, monocytes, and NK cells. Recent studies have demonstrated that CX3CL1–CX3CR1 interaction is associated with the development of various inflammatory skin diseases. In this study, we examined CX3CR1 involvement in 2,4-dinitrofluorobenzene (DNFB)-induced contact / hypersensitivity using CX3CR1− − mice. Ear swelling and dermal edema were attenuated after / DNFB challenge in CX3CR1− − mice. Expression of TNF-α, IL-6, and M1 macrophage markers / was decreased in the ears of CX3CR1− − mice, whereas expression of M2 macrophage markers including arginase-1 was increased. -
Critical Role of CXCL4 in the Lung Pathogenesis of Influenza (H1N1) Respiratory Infection
ARTICLES Critical role of CXCL4 in the lung pathogenesis of influenza (H1N1) respiratory infection L Guo1,3, K Feng1,3, YC Wang1,3, JJ Mei1,2, RT Ning1, HW Zheng1, JJ Wang1, GS Worthen2, X Wang1, J Song1,QHLi1 and LD Liu1 Annual epidemics and unexpected pandemics of influenza are threats to human health. Lung immune and inflammatory responses, such as those induced by respiratory infection influenza virus, determine the outcome of pulmonary pathogenesis. Platelet-derived chemokine (C-X-C motif) ligand 4 (CXCL4) has an immunoregulatory role in inflammatory diseases. Here we show that CXCL4 is associated with pulmonary influenza infection and has a critical role in protecting mice from fatal H1N1 virus respiratory infection. CXCL4 knockout resulted in diminished viral clearance from the lung and decreased lung inflammation during early infection but more severe lung pathology relative to wild-type mice during late infection. Additionally, CXCL4 deficiency decreased leukocyte accumulation in the infected lung with markedly decreased neutrophil infiltration into the lung during early infection and extensive leukocyte, especially lymphocyte accumulation at the late infection stage. Loss of CXCL4 did not affect the activation of adaptive immune T and B lymphocytes during the late stage of lung infection. Further study revealed that CXCL4 deficiency inhibited neutrophil recruitment to the infected mouse lung. Thus the above results identify CXCL4 as a vital immunoregulatory chemokine essential for protecting mice against influenza A virus infection, especially as it affects the development of lung injury and neutrophil mobilization to the inflamed lung. INTRODUCTION necrosis factor (TNF)-a, interleukin (IL)-6, and IL-1b, to exert Influenza A virus (IAV) infections cause respiratory diseases in further antiviral innate immune effects.2 Meanwhile, the innate large populations worldwide every year and result in seasonal immune cells act as antigen-presenting cells and release influenza epidemics and unexpected pandemic. -
Treatment with an Anti-CX3CL1 Antibody Suppresses M1 Macrophage Infiltration in Interstitial Lung Disease in SKG Mice
pharmaceuticals Article Treatment with an Anti-CX3CL1 Antibody Suppresses M1 Macrophage Infiltration in Interstitial Lung Disease in SKG Mice Satoshi Mizutani 1 , Junko Nishio 1,2, Kanoh Kondo 1, Kaori Motomura 1, Zento Yamada 1, Shotaro Masuoka 1, Soichi Yamada 1, Sei Muraoka 1 , Naoto Ishii 3, Yoshikazu Kuboi 3, Sho Sendo 4, Tetuo Mikami 5, Toshio Imai 3 and Toshihiro Nanki 1,* 1 Department of Internal Medicine, Division of Rheumatology, Toho University School of Medicine, Ota-ku, Tokyo 143-8541, Japan; [email protected] (S.M.); [email protected] (J.N.); [email protected] (K.K.); [email protected] (K.M.); [email protected] (Z.Y.); [email protected] (S.M.); [email protected] (S.Y.); [email protected] (S.M.) 2 Department of Immunopathology and Immunoregulation, Toho University School of Medicine, Ota-ku, Tokyo 143-8540, Japan 3 KAN Research Institute, Inc., Chuo-ku, Kobe-shi, Hyogo 650-0047, Japan; [email protected] (N.I.); [email protected] (Y.K.); [email protected] (T.I.) 4 Department of Internal Medicine, Division of Rheumatology and Clinical Immunology, Kobe University Graduate School of Medicine, Chuo-ku, Kobe-shi, Hyogo 650-0017, Japan; [email protected] 5 Department of Pathology, Toho University School of Medicine, Ota-ku, Tokyo 143-8540, Japan; Citation: Mizutani, S.; Nishio, J.; [email protected] Kondo, K.; Motomura, K.; Yamada, Z.; * Correspondence: [email protected]; Tel.: +81-3-3762-4151 (ext. -
Tissue-Specific Role of CX3CR1 Expressing Immune Cells and Their Relationships with Human Disease
Immune Netw. 2018 Feb;18(1):e5 https://doi.org/10.4110/in.2018.18.e5 pISSN 1598-2629·eISSN 2092-6685 Review Article Tissue-specific Role of CX3CR1 Expressing Immune Cells and Their Relationships with Human Disease Myoungsoo Lee1,2, Yongsung Lee1, Jihye Song1, Junhyung Lee1, Sun-Young Chang1,2,* 1Laboratory of Microbiology, College of Pharmacy, Ajou University, Suwon 16499, Korea 2Research Institute of Pharmaceutical Science and Technology (RIPST), Ajou University, Suwon 16499, Korea Received: Oct 14, 2017 ABSTRACT Revised: Dec 31, 2017 Accepted: Jan 1, 2018 Chemokine (C-X3-C motif ) ligand 1 (CX3CL1, also known as fractalkine) and its receptor *Correspondence to chemokine (C-X3-C motif ) receptor 1 (CX3CR1) are widely expressed in immune cells and Sun-Young Chang non-immune cells throughout organisms. However, their expression is mostly cell type- Laboratory of Microbiology, College of specific in each tissue. CX3CR1 expression can be found in monocytes, macrophages, Pharmacy, Ajou University, 164 World cup-ro, dendritic cells, T cells, and natural killer (NK) cells. Interaction between CX3CL1 and CX3CR1 Yeongtong-gu, Suwon 16499, Korea. can mediate chemotaxis of immune cells according to concentration gradient of ligands. E-mail: [email protected] CX3CR1 expressing immune cells have a main role in either pro-inflammatory or anti- Copyright © 2018. The Korean Association of inflammatory response depending on environmental condition. In a given tissue such as Immunologists bone marrow, brain, lung, liver, gut, and cancer, CX3CR1 expressing cells can maintain tissue This is an Open Access article distributed homeostasis. Under pathologic conditions, however, CX3CR1 expressing cells can play a under the terms of the Creative Commons Attribution Non-Commercial License (https:// critical role in disease pathogenesis. -
Ncomms1239.Pdf
ARTICLE Received 10 Nov 2010 | Accepted 15 Feb 2011 | Published 15 Mar 2011 DOI: 10.1038/ncomms1239 Inflammation driven by tumour-specific Th1 cells protects against B-cell cancer Ole Audun Werner Haabeth1, Kristina Berg Lorvik1, Clara Hammarström2, Ian M. Donaldson3,4, Guttorm Haraldsen2, Bjarne Bogen1 & Alexandre Corthay1 The immune system can both promote and suppress cancer. Chronic inflammation and proinflammatory cytokines such as interleukin (IL)-1 and IL-6 are considered to be tumour promoting. In contrast, the exact nature of protective antitumour immunity remains obscure. Here, we quantify locally secreted cytokines during primary immune responses against myeloma and B-cell lymphoma in mice. Strikingly, successful cancer immunosurveillance mediated by tumour-specific CD4 + T cells is consistently associated with elevated local levels of both proinflammatory (IL-1α, IL-1β and IL-6) and T helper 1 (Th1)-associated cytokines (interferon-γ (IFN-γ), IL-2 and IL-12). Cancer eradication is achieved by a collaboration between tumour- specific Th1 cells and tumour-infiltrating, antigen-presenting macrophages. Th1 cells induce secretion of IL-1β and IL-6 by macrophages. Th1-derived IFN-γ is shown to render macrophages directly cytotoxic to cancer cells, and to induce macrophages to secrete the angiostatic chemokines CXCL9/MIG and CXCL10/IP-10. Thus, inflammation, when driven by tumour- specific Th1 cells, may prevent rather than promote cancer. 1 Centre for Immune Regulation, Institute of Immunology, University of Oslo and Oslo University Hospital Rikshospitalet, PO Box 4950 Nydalen, 0424 Oslo, Norway. 2 Department of Pathology, Institute of Pathology, Oslo University Hospital Rikshospitalet and University of Oslo, PO Box 4950 Nydalen, 0424 Oslo, Norway. -
Fractalkine/CX3CL1 Via P38 MAPK Enhances the Adhesion Of
The CC Chemokine MCP-1 Stimulates Surface Expression of CX3CR1 and Enhances the Adhesion of Monocytes to Fractalkine/CX3CL1 via p38 MAPK This information is current as of September 25, 2021. Simone R. Green, Ki Hoon Han, Yiming Chen, Felicidad Almazan, Israel F. Charo, Yury I. Miller and Oswald Quehenberger J Immunol 2006; 176:7412-7420; ; doi: 10.4049/jimmunol.176.12.7412 Downloaded from http://www.jimmunol.org/content/176/12/7412 References This article cites 52 articles, 29 of which you can access for free at: http://www.jimmunol.org/ http://www.jimmunol.org/content/176/12/7412.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 25, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology The CC Chemokine MCP-1 Stimulates Surface Expression of CX3CR1 and Enhances the Adhesion of Monocytes to Fractalkine/CX3CL1 via p38 MAPK1 Simone R. -
Establishment of HIV-1 Latency in Resting CD4+ T Cells Depends on Chemokine-Induced Changes in the Actin Cytoskeleton
Establishment of HIV-1 latency in resting CD4+ T cells depends on chemokine-induced changes in the actin cytoskeleton Paul U. Camerona,b,c,1, Suha Salehb,1, Georgina Sallmannb, Ajantha Solomonb, Fiona Wightmanb, Vanessa A. Evansb, Genevieve Boucherd, Elias K. Haddadd,Rafick-Pierre Sekalyd, Andrew N. Harmane, Jenny L. Andersonf, Kate L. Jonesf, Johnson Makf,g, Anthony L. Cunninghame, Anthony Jaworowskib,c,f, and Sharon R. Lewina,b,f,2 aInfectious Diseases Unit, Alfred Hospital, Melbourne, Victoria 3004, Australia; Departments of bMedicine and cImmunology, Monash University, Melbourne 3004, Australia; dLaboratoire d’Immunologie, Centre de Recherche de Centre Hospitalier de L’Universitie de Montreal, Saint-Luc, Quebec, Canada; eWestmead Millenium Research Institute, Westmead 2145, Australia; fCentre for Virology, Burnet Institute, Melbourne 3004, Australia; and gDepartment of Biochemistry and Molecular Biology, Department of Microbiology, Monash University, Clayton 3800, Australia Edited by Malcolm A. Martin, National Institute of Allergy and Infectious Diseases, Bethesda, MD, and approved August 23, 2010 (received for review March 8, 2010) Eradication of HIV-1 with highly active antiretroviral therapy mokines, in addition to CXCR4 ligands may facilitate HIV-1 + (HAART) is not possible due to the persistence of long-lived, entry and integration in resting CD4 T cells and that this was latently infected resting memory CD4+ T cells. We now show that mediated via activation of actin. + HIV-1 latency can be established in resting CD4+ T cells infected We now show that the exposure of resting CD4 T cells to with HIV-1 after exposure to ligands for CCR7 (CCL19), CXCR3 the chemokines CCL19, CXCL10, and CCL20, all of which fi (CXCL9 and CXCL10), and CCR6 (CCL20) but not in unactivated regulate T-cell migration, allows for ef cient HIV-1 nuclear lo- + calization and integration of the HIV-1 provirus, that this oc- CD4 T cells. -
Chemokines and Their Receptors in Rheumatoid Arthritis
ARTHRITIS & RHEUMATISM Vol. 52, No. 3, March 2005, pp 710–721 DOI 10.1002/art.20932 © 2005, American College of Rheumatology REVIEW Chemokines and Their Receptors in Rheumatoid Arthritis Future Targets? Alisa E. Koch Introduction tem was introduced in 2000, in which chemokines are considered as chemokine ligands, and each chemokine Rheumatoid arthritis (RA) is a chronic inflam- has been assigned a designation of CXCL, CCL, XCL, matory disease leading to joint destruction (1). In RA, or CX3CL1 (Figure 1) (10–12). In this report, both the migration of leukocytes into the synovial tissue (ST) former and new nomenclature are noted. occurs. These leukocytes and other cells in the ST, particularly RA ST fibroblasts, produce mediators of CXC chemokines have 2 conserved cysteines inflammation, including chemokines (1). Chemokines, separated by 1 unconserved amino acid (9,13) (Figure currently numbering more than 50, are chemotactic 1). CXC chemokines classically were thought to be cytokines that are important in recruitment of leuko- involved in the chemotaxis of neutrophils. Many chemo- cytes and angiogenesis. They exert chemotactic activity kines may have arisen from reduplication of ancestral toward a variety of cell types (2–7). Some chemokines, genes (13). Hence, CXC chemokines that act on neutro- particularly CXC chemokines containing the ELR motif, phils are clustered on chromosome 4q12–13 (13). How- are angiogenic. The last few years have seen a rapid ever, some genes of more newly discovered CXC che- development of studies aimed at targeting proinflamma- mokines that recruit lymphocytes tend to be located tory chemokines or their receptors in RA and animal away from the major clusters (13). -
Expression and Analysis of CXCL8 and CXCL10 Chemokines In
erial D act is b ea o s c e y s M Mycobacterial Diseases Rawat et al., Mycobact Dis 2016, 6:2 DOI: 10.4172/2161-1068.1000208 ISSN: 2161-1068 Research an open access journal Expression and Analysis of CXCL8 and CXCL10 Chemokines in Human Skin Lesions Infected with M.leprae Krishan Dutta Rawat1, Mamta Chahar1, PVJ Reddy1, Nalini Srivastava2, U.D.Gupta1, M. Natrajan1, V.M. Katoch3, Kiran Katoch1 and D.S. Chauhan1* 1National JALMA Institute for Leprosy & Other Mycobacterial Diseases Tajganj, Agra, U.P, India 2SOS in Biotechnology, Jiwaji University, Gwalior, M.P, India. 3Department of Health Research, Indian Council of Medical Research, Ansari Nagar, New Delhi, India *Corresponding author: Chauhan DS, Microbiology & Molecular biology Lab, National JALMA Institute for Leprosy and Other Mycobacterial Diseases, (ICMR) Tajganj, Agra-282001, Tel: (0562) 2331751-4; Fax: +91-562-2331755; E-mail: [email protected] Rec date: February 02, 2016; Acc date: May 19, 2016; Pub date: May 24, 2016 Copyright: © 2016 Rawat KD, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract This study is focused to analyze the expression profile of CXCL8 and CXCL10 chemokines genes and to address the contribution of these chemokines in late phase of M.leprae infection in human skin lesion samples. In this study skin biopsy samples from leprosy patients (n=35) were collected including BL-LL=12, BB=14, BT=8 and healthy volunteers (n=3).