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CCL19-Igg Prevents Allograft Rejection by Impairment of Immune Cell Trafficking
CCL19-IgG Prevents Allograft Rejection by Impairment of Immune Cell Trafficking Ekkehard Ziegler,* Faikah Gueler,† Song Rong,† Michael Mengel,‡ Oliver Witzke,§ Andreas Kribben,§ Hermann Haller,† Ulrich Kunzendorf,* and Stefan Krautwald* *Department of Nephrology and Hypertension, University of Kiel, Kiel, †Department of Internal Medicine and ‡Institute for Pathology, Hannover Medical School, Hannover, and §Department of Nephrology, School of Medicine, University of Duisburg-Essen, Essen, Germany An adaptive immune response is initiated in the T cell area of secondary lymphoid organs, where antigen-presenting dendritic cells may induce proliferation and differentiation in co-localized T cells after T cell receptor engagement. The chemokines CCL19 and CCL21 and their receptor CCR7 are essential in establishing dendritic cell and T cell recruitment and co- localization within this unique microenvironment. It is shown that systemic application of a fusion protein that consists of CCL19 fused to the Fc part of human IgG1 induces effects similar to the phenotype of CCR7؊/؊ animals, like disturbed accumulation of T cells and dendritic cells in secondary lymphoid organs. CCL19-IgG further inhibited their co-localization, which resulted in a marked inhibition of antigen-specific T cell proliferation. The immunosuppressive potency of CCL19-IgG was tested in vivo using murine models for TH1-mediated immune responses (delayed-type hypersensitivity) and for transplantation of different solid organs. In allogeneic kidney transplantation as well as heterotopic allogeneic heart transplantation in different strain combinations, allograft rejection was reduced and organ survival was significantly prolonged by treatment with CCL19-IgG compared with controls. This shows that in contrast to only limited prolongation of graft survival in CCR7 knockout models, the therapeutic application of a CCR7 ligand in a wild-type environment provides a benefit in terms of immunosuppression. -
T Cell Binding to Activated Dendritic Cells Cutting Edge
Cutting Edge: CCR4 Mediates Antigen-Primed T Cell Binding to Activated Dendritic Cells Meng-tse Wu, Hui Fang and Sam T. Hwang This information is current as J Immunol 2001; 167:4791-4795; ; of September 27, 2021. doi: 10.4049/jimmunol.167.9.4791 http://www.jimmunol.org/content/167/9/4791 Supplementary http://www.jimmunol.org/content/suppl/2001/10/11/167.9.4791.DC1 Downloaded from Material References This article cites 32 articles, 13 of which you can access for free at: http://www.jimmunol.org/content/167/9/4791.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 27, 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 © 2001 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. ● Cutting Edge: CCR4 Mediates Antigen-Primed T Cell Binding to Activated Dendritic Cells Meng-tse Wu, Hui Fang, and Sam T. Hwang1 DC. In the periphery, activated, Ag-bearing DC may bind to cog- The binding of a T cell to an Ag-laden dendritic cell (DC) is a nate effector memory T cells (mTC). -
Cells Effects on the Activation and Apoptosis of T Induces Opposing
Fibronectin-Associated Fas Ligand Rapidly Induces Opposing and Time-Dependent Effects on the Activation and Apoptosis of T Cells This information is current as of September 28, 2021. Alexandra Zanin-Zhorov, Rami Hershkoviz, Iris Hecht, Liora Cahalon and Ofer Lider J Immunol 2003; 171:5882-5889; ; doi: 10.4049/jimmunol.171.11.5882 http://www.jimmunol.org/content/171/11/5882 Downloaded from References This article cites 40 articles, 17 of which you can access for free at: http://www.jimmunol.org/content/171/11/5882.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 28, 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 © 2003 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Fibronectin-Associated Fas Ligand Rapidly Induces Opposing and Time-Dependent Effects on the Activation and Apoptosis of T Cells1 Alexandra Zanin-Zhorov, Rami Hershkoviz, Iris Hecht, Liora Cahalon, and Ofer Lider2 Recently, it has been shown that Fas ligand (FasL) interacts with the extracellular matrix (ECM) protein fibronectin (FN), and that the bound FasL retains its cytotoxic efficacy. -
Following Ligation of CCL19 but Not CCL21 Arrestin 3 Mediates
Arrestin 3 Mediates Endocytosis of CCR7 following Ligation of CCL19 but Not CCL21 Melissa A. Byers, Psachal A. Calloway, Laurie Shannon, Heather D. Cunningham, Sarah Smith, Fang Li, Brian C. This information is current as Fassold and Charlotte M. Vines of September 25, 2021. J Immunol 2008; 181:4723-4732; ; doi: 10.4049/jimmunol.181.7.4723 http://www.jimmunol.org/content/181/7/4723 Downloaded from References This article cites 82 articles, 45 of which you can access for free at: http://www.jimmunol.org/content/181/7/4723.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 25, 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 © 2008 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Arrestin 3 Mediates Endocytosis of CCR7 following Ligation of CCL19 but Not CCL211 Melissa A. Byers,* Psachal A. Calloway,* Laurie Shannon,* Heather D. Cunningham,* Sarah Smith,* Fang Li,† Brian C. -
Mechanism of Macrophage-Derived Chemokine/CCL22 Production by Hacat Keratinocytes
C Yano, et al Ann Dermatol Vol. 27, No. 2, 2015 http://dx.doi.org/10.5021/ad.2015.27.2.152 ORIGINAL ARTICLE Mechanism of Macrophage-Derived Chemokine/CCL22 Production by HaCaT Keratinocytes Chizuko Yano, Hidehisa Saeki1, Mayumi Komine2, Shinji Kagami3, Yuichiro Tsunemi4, Mamitaro Ohtsuki2, Hidemi Nakagawa Department of Dermatology, The Jikei University School of Medicine, 1Department of Dermatology, Nippon Medical School, Tokyo, 2Department of Dermatology, Jichi Medical University, Shimotsuke, 3Department of Dermatology, Kanto Central Hospital, 4Department of Dermatology, Tokyo Women’s Medical University, Tokyo, Japan Background: CC chemokine ligand 17 (CCL17) and CCL22 27(2) 152∼156, 2015) are the functional ligands for CCR4. We previously reported that inhibitors of nuclear factor-kappa B and p38 mi- -Keywords- togen-activated protein kinase (p38 MAPK), but not of ex- Chemokine CCL22, Chemokine CCL17, Epidermal growth tracellular signal-related kinase (ERK), inhibited tumor ne- factor receptor, HaCaT keratinocytes crosis factor (TNF)-α- and interferon (IFN)-γ-induced pro- duction of CCL17 by the human keratinocyte cell line, HaCaT. Further, an inhibitor of epidermal growth factor re- INTRODUCTION ceptor (EGFR) enhanced the CCL17 production by these keratinocytes. Objective: To identify the mechanism under- The macrophage-derived chemokine (MDC)/CC chemo- lying CCL22 production by HaCaT cells. Methods: We inves- kine ligand 22 (CCL22) is one of the functional ligands for tigated the signal transduction pathways by which TNF-α CC chemokine receptor 4 (CCR4) and is a chemoattractant and IFN-γ stimulate HaCaT cells to produce CCL22 by add- for the CCR4-expressing cells such as Th2 cells. We and ing various inhibitors. -
Differential Expression of Interferon-Γ and Chemokine Genes
Differential expression of interferon-γ and chemokine genes distinguishes Rasmussen encephalitis from cortical dysplasia and provides evidence for an early Th1 immune response Owens et al. Owens et al. Journal of Neuroinflammation 2013, 10:56 http://www.jneuroinflammation.com/content/10/1/56 Owens et al. Journal of Neuroinflammation 2013, 10:56 JOURNAL OF http://www.jneuroinflammation.com/content/10/1/56 NEUROINFLAMMATION RESEARCH Open Access Differential expression of interferon-γ and chemokine genes distinguishes Rasmussen encephalitis from cortical dysplasia and provides evidence for an early Th1 immune response Geoffrey C Owens1,7*, My N Huynh1, Julia W Chang1, David L McArthur1, Michelle J Hickey2, Harry V Vinters2,3, Gary W Mathern1,4,5,6† and Carol A Kruse1,6† Abstract Background: Rasmussen encephalitis (RE) is a rare complex inflammatory disease, primarily seen in young children, that is characterized by severe partial seizures and brain atrophy. Surgery is currently the only effective treatment option. To identify genes specifically associated with the immunopathology in RE, RNA transcripts of genes involved in inflammation and autoimmunity were measured in brain tissue from RE surgeries and compared with those in surgical specimens of cortical dysplasia (CD), a major cause of intractable pediatric epilepsy. Methods: Quantitative polymerase chain reactions measured the relative expression of 84 genes related to inflammation and autoimmunity in 12 RE specimens and in the reference group of 12 CD surgical specimens. Data were analyzed by consensus clustering using the entire dataset, and by pairwise comparison of gene expression levels between the RE and CD cohorts using the Harrell-Davis distribution-free quantile estimator method. -
Inhibition of CCL19 Benefits Non‑Alcoholic Fatty Liver Disease by Inhibiting TLR4/NF‑Κb‑P65 Signaling
MOLECULAR MEDICINE REPORTS 18: 4635-4642, 2018 Inhibition of CCL19 benefits non‑alcoholic fatty liver disease by inhibiting TLR4/NF‑κB‑p65 signaling JIAJING ZHAO1*, YINGJUE WANG1*, XI WU2, PING TONG3, YAOHAN YUE1, SHURONG GAO1, DONGPING HUANG4 and JIANWEI HUANG4 1Department of Traditional Chinese Medicine, Putuo District People's Hospital of Shanghai City, Shanghai 200060; 2Department of Endocrinology, Huashan Hospital, Fu Dan University, Shanghai 200040; Departments of 3Endocrinology and 4General Surgery, Putuo District People's Hospital of Shanghai City, Shanghai 200060, P.R. China Received January 26, 2018; Accepted August 21, 2018 DOI: 10.3892/mmr.2018.9490 Abstract. Non-alcoholic fatty liver disease (NAFLD), which that metformin and BBR could improve NAFLD, which may be affects approximately one-third of the general population, has via the activation of AMPK signaling, and the high expression of become a global health problem. Thus, more effective treatments CCL19 in NAFLD was significantly reduced by metformin and for NAFLD are urgently required. In the present study, high BBR. It could be inferred that inhibition of CCL19 may be an levels of C-C motif ligand 19 (CCL19), signaling pathways such effective treatment for NAFLD. as Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB), and proinflammatory factors including interleukin‑6 (IL‑6) and tumor Introduction necrosis factor-α (TNF-α) were detected in NAFLD patients, thereby indicating that there may be an association between Fatty liver diseases, whose prevalence is continuously rising CCL19 and these factors in NAFLD progression. Using a high-fat worldwide, especially in developed countries, are character- diet (HFD), the present study generated a Sprague-Dawley rat ized by excessive hepatic fat accumulation (1). -
Mice in Inflammation Psoriasiform Skin IL-22 Is Required for Imiquimod-Induced
IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle, Magali de Heusch, Muriel M. Lemaire, Emilie Hendrickx, Guy Warnier, Kyri This information is current as Dunussi-Joannopoulos, Lynette A. Fouser, Jean-Christophe of September 29, 2021. Renauld and Laure Dumoutier J Immunol published online 30 November 2011 http://www.jimmunol.org/content/early/2011/11/30/jimmun ol.1102224 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 Copyright © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published November 30, 2011, doi:10.4049/jimmunol.1102224 The Journal of Immunology IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle,*,† Magali de Heusch,*,† Muriel M. Lemaire,*,† Emilie Hendrickx,*,† Guy Warnier,*,† Kyri Dunussi-Joannopoulos,‡ Lynette A. Fouser,‡ Jean-Christophe Renauld,*,†,1 and Laure Dumoutier*,†,1 Psoriasis is a common chronic autoimmune skin disease of unknown cause that involves dysregulated interplay between immune cells and keratinocytes. -
CXCL13/CXCR5 Signaling Axis in Cancer
Life Sciences 227 (2019) 175–186 Contents lists available at ScienceDirect Life Sciences journal homepage: www.elsevier.com/locate/lifescie Review article CXCL13/CXCR5 signaling axis in cancer T ⁎ Muzammal Hussaina,b,1, Dickson Adahb,c,1, Muqddas Tariqa,b, Yongzhi Lua, Jiancun Zhanga, , ⁎ Jinsong Liua, a Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, 190 Kaiyuan Avenue, Science Park, Guangzhou 510530, PR China b University of Chinese Academy of Sciences, Beijing 100049, PR China c State Key Laboratory of Respiratory Disease, Center for Infection and Immunity, Guangzhou Institutes of Biomedicine and Heath, Chinese Academy of Sciences, 190 Kaiyuan Avenue, Science Park, Guangzhou 510530, PR China ARTICLE INFO ABSTRACT Keywords: The tumor microenvironment comprises stromal and tumor cells which interact with each other through com- Cancer plex cross-talks that are mediated by a variety of growth factors, cytokines, and chemokines. The chemokine CXCL13 ligand 13 (CXCL13) and its chemokine receptor 5 (CXCR5) are among the key chemotactic factors which play CXCR5 crucial roles in deriving cancer cell biology. CXCL13/CXCR5 signaling axis makes pivotal contributions to the Tumor progression development and progression of several human cancers. In this review, we discuss how CXCL13/CXCR5 sig- Tumor immunity naling modulates cancer cell ability to grow, proliferate, invade, and metastasize. Furthermore, we also discuss Immune-evasion the preliminary evidence on context-dependent functioning of this axis within the tumor-immune micro- environment, thus, highlighting its potential dichotomy with respect to anticancer immunity and cancer im- mune-evasion mechanisms. At the end, we briefly shed light on the therapeutic potential or implications of targeting CXCL13/CXCR5 axis within the tumor microenvironment. -
Rescuing Functional T Cells Induced by Growth Factor Deprivation, CCL2 Inhibits the Apoptosis Program
CCL2 Inhibits the Apoptosis Program Induced by Growth Factor Deprivation, Rescuing Functional T Cells This information is current as Eva Diaz-Guerra, Rolando Vernal, M. Julieta del Prete, of September 24, 2021. Augusto Silva and Jose A. Garcia-Sanz J Immunol 2007; 179:7352-7357; ; doi: 10.4049/jimmunol.179.11.7352 http://www.jimmunol.org/content/179/11/7352 Downloaded from References This article cites 41 articles, 21 of which you can access for free at: http://www.jimmunol.org/content/179/11/7352.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 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 © 2007 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology CCL2 Inhibits the Apoptosis Program Induced by Growth Factor Deprivation, Rescuing Functional T Cells1 Eva Diaz-Guerra,2 Rolando Vernal,2 M. Julieta del Prete,2 Augusto Silva, and Jose A. Garcia-Sanz3 The precise mechanisms involved in the switch between the clonal expansion and contraction phases of a CD8؉ T cell response remain to be fully elucidated. -
Ccl17-Dependent Release of Ccl3 Restrains Regulatory T Cells Thereby Aggravating Atherosclerosis
From the Institute for Cardiovascular Prevention (IPEK) of the Ludwig-Maximilians-Universität München Director: Univ.-Prof. Dr. med. Christian Weber Ccl17-dependent release of Ccl3 restrains regulatory T cells thereby aggravating atherosclerosis Dissertation zum Erwerb des Doctor of Philosophy (Ph.D.) an der Medizinischen Fakultät der Ludwig-Maximilians-Universität München Submitted by M.Sc. Carlos Neideck from Taió in Santa Catarina, Brazil on 21.03.2018 Supervisor: Prof. Dr. med. Christian Weber Second evaluator: Prof. Dr. rer. nat. Jürgen Bernhagen Dean: Prof. Dr. Reinhard Hickel Date of oral defense: 23.07.2018 Affidavit Neideck, Carlos ______________________________________________________________________ Name, Surname ______________________________________________________________________ Street ______________________________________________________________________ Zip Code, Town ______________________________________________________________________ Country I hereby declare, that the submitted thesis entitled: “Ccl17-dependent release of Ccl3 restrains regulatory T cells thereby aggravating atherosclerosis.” is my own work. I have only used the sources indicated and have not made unauthorized use of services of a third party. Where the work of others has been quoted or reproduced, the source is always given. I further declare that the submitted thesis or parts thereof have not been presented as part of an examination degree to any other university. Munich, 25.07.2018 Carlos Neideck Place, date Signature doctoral candidate Confirmation -
Interleukin-15-Mediated Immunotoxicity and Exacerbation of Sepsis
INTERLEUKIN-15-MEDIATED IMMUNOTOXICITY AND EXACERBATION OF SEPSIS: ROLE OF NATURAL KILLER CELLS AND INTERFERON γ By Yin Guo Dissertation Submitted to the Faculty of the Graduate School of Vanderbilt University in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY in Microbiology and Immunology December 2016 Nashville, Tennessee Approved Luc Van Kaer, Ph.D. Stokes Peebles, M.D. Lorraine Ware, M.D. Daniel Moore, M.D., Ph.D. Edward Sherwood, M.D, Ph.D. i Copyright © 2016 by Yin Guo All Rights Reserved ii ACKNOWLEDGEMENTS I would like to thank my thesis mentor, Dr. Edward Sherwood for his tremendous instruction and support during my entire Ph.D. training course. I joined Dr. Sherwood’s lab in the department of Microbiology and Immunology of University of Texas Medical Branch (UTMB) at Galveston in 2011. I appreciated the offer Dr. Sherwood provided to move to Vanderbilt University together. During the new lab setup period, he gave me a lot of encouragement about going out to meet students and professors at the Pathology, Microbiology and Immunology Department. From making new friends in our department, I started to know a lot of useful information and resources about how to adapt to new life in Nashville and how to prepare for the qualifying exam. Dr. Sherwood is a highly responsible and enthusiastic mentor although he has busy medical practice in the operating room and needs to write many grants. I have to say, he is the most diligent person I have seen in the world. It is amazing to me that he never seems to be exhausted or desensitized with reviewing our papers, reading papers, writing grants, and discussing data and new ideas.