Ccl9 Induced by Tgf-Β Signaling in Myeloid Cells Enhances Tumor Cell Survival in the Premetastatic Lung
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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. -
The Importance of Microenvironment: the Role of CCL8 in Metastasis Formation of Melanoma
www.impactjournals.com/oncotarget/ Oncotarget, Vol. 6, No. 30 The importance of microenvironment: the role of CCL8 in metastasis formation of melanoma Tamás Barbai1, Zsuzsanna Fejős1, Laszlo G. Puskas2, József Tímár1,3 and Erzsébet Rásó1,3 1 2nd Department of Pathology, Semmelweis University, Budapest, Hungary 2 Avidin Ltd., Szeged, Hungary 3 MTA-SE Tumor Progression Research Group, Budapest, Hungary Correspondence to: Tamás Barbai, email: [email protected] Keywords: melanoma metastasis, microenvironment, CCL8, miR146a Received: February 19, 2015 Accepted: July 16, 2015 Published: July 31, 2015 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 We have attempted to characterize the changes occurring on the host side during the progression of human melanoma. To investigate the role of tumor microenvironment, we set up such an animal model, which was able to isolate the host related factors playing central role in metastasis formation. One of these ’factors’, CCL12, was consequently selected and its behavior was examined alongside its human homologue (CCL8). In our animal model, metastasis forming primary melanoma in the host exhibited increased level of CCL12 mRNA expression. In clinical samples, when examining the tumor and the host together, the cumulative (tumor and host) CCL8 expression was lower in the group in which human primary melanoma formed lung metastasis compared to non-metastatic primary tumors. We could not detect significant difference in CCL8 receptor (CCR1) expression between the two groups. Increased migration of the examined tumor cell lines was observed when CCL8 was applied as a chemoattractant. -
CCL9 Is Secreted by the Follicle-Associated Epithelium and Recruits Dome Region Peyer's Patch Cd11b+ Dendritic Cells
CCL9 Is Secreted by the Follicle-Associated Epithelium and Recruits Dome Region Peyer's Patch CD11b+ Dendritic Cells This information is current as Xinyan Zhao, Ayuko Sato, Charles S. Dela Cruz, Melissa of October 1, 2021. Linehan, Andreas Luegering, Torsten Kucharzik, Aiko-Konno Shirakawa, Gabriel Marquez, Joshua M. Farber, Ifor Williams and Akiko Iwasaki J Immunol 2003; 171:2797-2803; ; doi: 10.4049/jimmunol.171.6.2797 http://www.jimmunol.org/content/171/6/2797 Downloaded from References This article cites 32 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/171/6/2797.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • 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 by guest on October 1, 2021 *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 Errata An erratum has been published regarding this article. Please see next page or: /content/172/11/7220.2.full.pdf 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 © 2003 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology CCL9 Is Secreted by the Follicle-Associated Epithelium and Recruits Dome Region Peyer’s Patch CD11b؉ Dendritic Cells1 Xinyan Zhao,2* Ayuko Sato,* Charles S. -
Chemokine Signatures of Pathogen-Specific T Cells II: Memory T Cells in Acute and Chronic Infection
Chemokine Signatures of Pathogen-Specific T Cells II: Memory T Cells in Acute and Chronic Infection This information is current as Bennett Davenport, Jens Eberlein, Tom T. Nguyen, of September 24, 2021. Francisco Victorino, Verena van der Heide, Maxim Kuleshov, Avi Ma'ayan, Ross Kedl and Dirk Homann J Immunol published online 18 September 2020 http://www.jimmunol.org/content/early/2020/09/17/jimmun ol.2000254 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2020/09/17/jimmunol.200025 Material 4.DCSupplemental http://www.jimmunol.org/ Why The JI? Submit online. • 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 by guest on September 24, 2021 *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 © 2020 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published September 18, 2020, doi:10.4049/jimmunol.2000254 The Journal of Immunology Chemokine Signatures of Pathogen-Specific T Cells II: Memory T Cells in Acute and Chronic Infection Bennett Davenport,*,†,‡,x,{ Jens Eberlein,*,† Tom T. Nguyen,*,‡ Francisco Victorino,*,†,‡ Verena van der Heide,x,{ Maxim Kuleshov,‖,# Avi Ma’ayan,‖,# Ross Kedl,† and Dirk Homann*,†,‡,x,{ Pathogen-specific memory T cells (TM) contribute to enhanced immune protection under conditions of reinfection, and their effective recruitment into a recall response relies, in part, on cues imparted by chemokines that coordinate their spatiotemporal positioning. -
Chemokine and Chemokine Receptor Expression During Colony Stimulating Factor-1-Induced Osteoclast Differentiation in the Toothle
University of Massachusetts Medical School eScholarship@UMMS Open Access Articles Open Access Publications by UMMS Authors 2005-11-24 Chemokine and chemokine receptor expression during colony stimulating factor-1-induced osteoclast differentiation in the toothless osteopetrotic rat: a key role for CCL9 (MIP-1gamma) in osteoclastogenesis in vivo and in vitro Meilheng Yang University of Massachusetts Medical School Et al. Let us know how access to this document benefits ou.y Follow this and additional works at: https://escholarship.umassmed.edu/oapubs Part of the Cell Biology Commons Repository Citation Yang M, Mailhot G, MacKay CA, Mason-Savas A, Aubin J, Odgren PR. (2005). Chemokine and chemokine receptor expression during colony stimulating factor-1-induced osteoclast differentiation in the toothless osteopetrotic rat: a key role for CCL9 (MIP-1gamma) in osteoclastogenesis in vivo and in vitro. Open Access Articles. https://doi.org/10.1182/blood-2005-08-3365. Retrieved from https://escholarship.umassmed.edu/oapubs/275 This material is brought to you by eScholarship@UMMS. It has been accepted for inclusion in Open Access Articles by an authorized administrator of eScholarship@UMMS. For more information, please contact [email protected]. CHEMOKINES, CYTOKINES, AND INTERLEUKINS Chemokine and chemokine receptor expression during colony stimulating factor-1–induced osteoclast differentiation in the toothless osteopetrotic rat: a key role for CCL9 (MIP-1␥) in osteoclastogenesis in vivo and in vitro Meiheng Yang, Genevie`ve Mailhot, Carole A. MacKay, April Mason-Savas, Justin Aubin, and Paul R. Odgren Osteoclasts differentiate from hematopoi- peared on day 2, peaked on day 4, and oclasts on day 2 and in mature cells at etic precursors under systemic and local decreased slightly on day 6, as marrow later times. -
Macrophage-Derived CXCL9 and CXCL10 Are Required for Antitumor Immune Responses Following Immune Checkpoint Blockade a C Imran G
Published OnlineFirst October 21, 2019; DOI: 10.1158/1078-0432.CCR-19-1868 CLINICAL CANCER RESEARCH | TRANSLATIONAL CANCER MECHANISMS AND THERAPY Macrophage-Derived CXCL9 and CXCL10 Are Required for Antitumor Immune Responses Following Immune Checkpoint Blockade A C Imran G. House1,2, Peter Savas2,3, Junyun Lai1,2, Amanda X.Y. Chen1,2, Amanda J. Oliver1,2, Zhi L. Teo2,3, Kirsten L. Todd1,2, Melissa A. Henderson1,2, Lauren Giuffrida1,2, Emma V. Petley1,2, Kevin Sek1,2, Sherly Mardiana1,2, Tuba N. Gide4, Camelia Quek4, Richard A. Scolyer4,5, Georgina V. Long4,6,7, James S. Wilmott4, Sherene Loi2,3, Phillip K. Darcy1,2,8,9, and Paul A. Beavis1,2 ABSTRACT ◥ Purpose: Response rates to immune checkpoint blockade (ICB; single-cell RNA-sequencing (RNA-seq) and paired survival anti-PD-1/anti-CTLA-4) correlate with the extent of tumor analyses. immune infiltrate, but the mechanisms underlying the recruit- Results: The CXCR3 ligands, CXCL9 and CXCL10, were sig- ment of T cells following therapy are poorly characterized. A nificantly upregulated following dual PD-1/CTLA-4 blockade and þ greater understanding of these processes may see the develop- both CD8 T-cell infiltration and therapeutic efficacy were CXCR3 ment of therapeutic interventions that enhance T-cell recruit- dependent. In both murine models and patients undergoing immu- ment and, consequently, improved patient outcomes. We there- notherapy, macrophages were the predominant source of CXCL9 þ fore investigated the chemokines essential for immune cell and their depletion abrogated CD8 T-cell infiltration and the recruitment and subsequent therapeutic efficacy of these immu- therapeutic efficacy of dual ICB. -
Mixed Lineage Kinase 3 Inhibition Induces T Cell Activation and Cytotoxicity
Mixed lineage kinase 3 inhibition induces T cell activation and cytotoxicity Sandeep Kumara, Sunil Kumar Singha, Navin Viswakarmaa, Gautam Sondarvaa, Rakesh Sathish Naira, Periannan Sethupathia, Subhash C. Sinhab, Rajyasree Emmadic, Kent Hoskinsd, Oana Danciud, Gregory R. J. Thatchere, Basabi Ranaa,f,g, and Ajay Ranaa,f,g,1 aDepartment of Surgery, Division of Surgical Oncology, University of Illinois at Chicago, Chicago, IL 60612; bLaboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10065; cDepartment of Pathology, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612; dDivision of Hematology/Oncology, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612; eDepartment of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, IL 60612; fUniversity of Illinois Hospital and Health Sciences System Cancer Center, University of Illinois at Chicago, Chicago, IL 60612; and gResearch Unit, Jesse Brown VA Medical Center, Chicago, IL 60612 Edited by Michael Karin, University of California San Diego School of Medicine, La Jolla, CA, and approved February 26, 2020 (received for review December 5, 2019) Mixed lineage kinase 3 (MLK3), also known as MAP3K11, was cytotoxic effects of chemotherapeutic agents in estrogen receptor- + initially identified in a megakaryocytic cell line and is an emerging positive (ER ) breast cancer (3). We also reported that MLK3 is therapeutic target in cancer, yet its role in immune cells is not inhibited by human epidermal growth factor receptor 2 (HER2) known. Here, we report that loss or pharmacological inhibition amplification, and this allows HER2+ breast cancer cells to pro- of MLK3 promotes activation and cytotoxicity of T cells. -
Diverse and Potent Chemokine Production by Lung Cd11bhigh Dendritic Cells in Homeostasis and in Allergic Lung Inflammation
Diverse and Potent Chemokine Production by Lung CD11b high Dendritic Cells in Homeostasis and in Allergic Lung Inflammation This information is current as of September 29, 2021. Steven R. Beaty, C. Edward Rose, Jr. and Sun-sang J. Sung J Immunol 2007; 178:1882-1895; ; doi: 10.4049/jimmunol.178.3.1882 http://www.jimmunol.org/content/178/3/1882 Downloaded from References This article cites 69 articles, 42 of which you can access for free at: http://www.jimmunol.org/content/178/3/1882.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • 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 by guest on September 29, 2021 *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 © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Diverse and Potent Chemokine Production by Lung CD11bhigh Dendritic Cells in Homeostasis and in Allergic Lung Inflammation1 Steven R. Beaty, C. Edward Rose, Jr., and Sun-Sang J. Sung2 Lung CD11chigh dendritic cells (DC) are comprised of two major phenotypically distinct populations, the CD11bhigh DC and the ؉ ؉  ␣ integrin E 7 DC (CD103 DC). -
Chemokine Receptors and Chemokine Production by CD34+ Stem Cell-Derived Monocytes in Response to Cancer Cells
ANTICANCER RESEARCH 32: 4749-4754 (2012) Chemokine Receptors and Chemokine Production by CD34+ Stem Cell-derived Monocytes in Response to Cancer Cells MALGORZATA STEC, JAROSLAW BARAN, MONIKA BAJ-KRZYWORZEKA, KAZIMIERZ WEGLARCZYK, JOLANTA GOZDZIK, MACIEJ SIEDLAR and MAREK ZEMBALA Department of Clinical Immunology and Transplantation, Polish-American Institute of Paediatrics, Jagiellonian University Medical College, Cracow, Poland Abstract. Background: The chemokine-chemokine receptor The chemokine–chemokine receptor (CR) network is involved (CR) network is involved in the regulation of cellular in the regulation of leukocyte infiltration of tumours. infiltration of tumours. Cancer cells and infiltrating Leukocytes, including monocytes, migrate to the tumour via macrophages produce a whole range of chemokines. This the gradient of chemokines that are produced by tumour and study explored the expression of some CR and chemokine stromal cells, including monocyte-derived macrophages (1-4). production by cord blood stem cell-derived CD34+ Several chemokines are found in the tumour microenvironment monocytes and their novel CD14++CD16+ and and are involved in the regulation of tumour-infiltrating CD14+CD16– subsets in response to tumour cells. Material macrophages (TIMs), by controlling their directed migration to and Methods: CR expression was determined by flow the tumour and inhibiting their egress by regulation of cytometry and their functional activity by migration to angiogenesis and immune response to tumour cells and by chemoattractants. -
2079.Full.Pdf
Site-Specific Production of IL-6 in the Central Nervous System Retargets and Enhances the Inflammatory Response in Experimental Autoimmune This information is current as Encephalomyelitis of September 26, 2021. Albert Quintana, Marcus Müller, Ricardo F. Frausto, Raquel Ramos, Daniel R. Getts, Elisenda Sanz, Markus J. Hofer, Marius Krauthausen, Nicholas J. C. King, Juan Hidalgo and Iain L. Campbell Downloaded from J Immunol 2009; 183:2079-2088; Prepublished online 13 July 2009; doi: 10.4049/jimmunol.0900242 http://www.jimmunol.org/content/183/3/2079 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2009/07/14/jimmunol.090024 Material 2.DC1 References This article cites 50 articles, 15 of which you can access for free at: http://www.jimmunol.org/content/183/3/2079.full#ref-list-1 by guest on September 26, 2021 Why The JI? Submit online. • 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 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 © 2009 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. -
Mucosal Immunity Learning Goal
Host Defense 2012 Mucosal Immunity April 18, 2012 Katherine L.Knight, Ph.D. MUCOSAL IMMUNITY LEARNING GOAL You will be able to describe the mucosal immune system. OBJECTIVES To attain the goal for these lectures you will be able to: • Describe the components of the mucosal immune system. • Describe the structure of secretory IgA. • Explain the mechanism of IgA transport across mucosal surfaces. • Explain how a response to antigen is generated in the mucosal system. • Identify the differences in tolerogenic versus immunogenic responses to mucosal antigen administration. • Delineate the functions of the mucosal immune system, including M cells. • Describe how the mucosal immune system might be used for immunization. • Describe the characteristics of selective IgA deficiency. • Describe how intestinal commensal bacteria interact with the host to promote a healthy environment READING ASSIGNMENT Janeway, et. al., (2008), Chapter 11, and Article “Mucosal Vaccines: the Promise and the Challenge” by Marian R. Neutra and Pamela A. Kozlowski, attached at end of lecture notes. LECTURER Katherine L. Knight, Ph.D. Page 1 Host Defense 2012 Mucosal Immunity April 18, 2012 Katherine L.Knight, Ph.D. CONTENT SUMMARY I. INTRODUCTION TO MUCOSAL IMMUNITY II. ORGANIZATION OF THE MUCOSAL IMMUNE SYSTEM A. Components of the Mucosal Immune System B. Induction of a Response C. Features of Mucosal Immunity D. Intraepithelial lymphocytes (IEL) III. IgA SYNTHESIS, STRUCTURE AND TRANSPORT IV. FUNCTIONS OF IgA AT MUCOSAL SURFACES A. Barrier Functions B. Intraepithelial Viral Neutralization C. Excretory Immunity D. Passive Immunity E. IgA Deficiency State V. MUCOSAL IMMUNIZATION VI. MUCOSAL TOLERANCE A. The Induction of Tolerance via Mucosal Sites B. -
Successful Immunotherapy with IL-2/Anti-CD40 Induces the Chemokine-Mediated Mitigation of an Immunosuppressive Tumor Microenvironment
Successful immunotherapy with IL-2/anti-CD40 induces the chemokine-mediated mitigation of an immunosuppressive tumor microenvironment Jonathan M. Weissa, Timothy C. Backa, Anthony J. Scarzelloa, Jeff J. Subleskia, Veronica L. Halla, Jimmy K. Stauffera, Xin Chena, Dejan Micica, Kory Aldersonb, William J. Murphyb, and Robert H. Wiltrouta,1 aLaboratory of Experimental Immunology, Cancer and Inflammation Program, NCI Frederick, Frederick, MD 21702; and bDepartment of Dermatology, University of California, Davis, CA 95616 Edited by Thomas A. Waldmann, National Institutes of Health, Bethesda, MD, and approved September 28, 2009 (received for review August 25, 2009) Treatment of mice bearing orthotopic, metastatic tumors with associated with the recruitment of mononuclear cells capable of anti-CD40 antibody resulted in only partial, transient anti-tumor producing tumor promoting factors (8, 9), as well as MDSC that effects whereas combined treatment with IL-2/anti-CD40, induced contribute to tumor progression through the inhibition of effec- tumor regression. The mechanisms for these divergent anti-tumor tor cell functions (8, 10). responses were examined by profiling tumor-infiltrating leukocyte We reported previously that IL-2 and agonistic antibody to subsets and chemokine expression within the tumor microenvi- CD40 (␣CD40) synergize for the regression of metastatic tumors ronment after immunotherapy. IL-2/anti-CD40, but not anti-CD40 in mice (11). Although we identified CD8ϩ T cells and host IFN␥ alone, induced significant infiltration of established tumors by NK expression as critical components of this therapeutic approach -and CD8؉ T cells. To further define the role of chemokines in (11), the specific mechanisms underlying the IL-2/␣CD40 syn leukocyte recruitment into tumors, we evaluated anti-tumor re- ergistic anti-tumor responses within the microenvironment re- sponses in mice lacking the chemokine receptor, CCR2.