Polyclonal Anti-CCR1 Antibody
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Role of Chemokines and Chemokine Receptors in Shaping the Effector Phase of the Antitumor Immune Response
Published OnlineFirst December 7, 2012; DOI: 10.1158/0008-5472.CAN-12-2027 Cancer Review Research Role of Chemokines and Chemokine Receptors in Shaping the Effector Phase of the Antitumor Immune Response Katarzyna Franciszkiewicz1, Alexandre Boissonnas2, Marie Boutet1, Christophe Combadiere 2, and Fathia Mami-Chouaib1 Abstract Immune system–mediated eradication of neoplastic cells requires induction of a strong long-lasting antitumor T-cell response. However, generation of tumor-specific effector T cells does not necessarily result in tumor clearance. CTL must firstbeabletomigratetothetumorsite,infiltrate the tumor tissue, and interact with the target to finally trigger effector functions indispensable for tumor destruction. Chemokines are involved in circulation, homing, retention, and activation of immunocompetent cells. Although some of them are known to contribute to tumor growth and metastasis, others are responsible for changes in the tumor microenvironment that lead to extensive infiltration of lymphocytes, resulting in tumor eradication. Given their chemoattractive and activating properties, a role for chemokines in the development of the effector phase of the antitumor immune response has been suggested. Here, we emphasize the role of the chemokine–chemokine receptor network at multiple levels of the T-cell–mediated antitumor immune response. The identification of chemokine-dependent molecular mechanisms implicated in tumor-specific CTL trafficking, retention, and regulation of their in situ effector functions may offer new perspectives for development of innovative immunotherapeutic approaches to cancer treatment. Cancer Res; 72(24); 1–8. Ó2012 AACR. Introduction critical step in optimization of current cancer immunotherapy The identification of tumor-associated antigens (TAA) and protocols. the isolation of tumor-specific cytotoxic T cells have led to Chemokines coordinate circulation, homing, and retention great efforts in developing immunotherapeutic approaches to of immune cells. -
Th2 Effector Lymphocytes Regulatory and + Cells Enriched for FOXP3
CCR8 Expression Identifies CD4 Memory T Cells Enriched for FOXP3 + Regulatory and Th2 Effector Lymphocytes This information is current as Dulce Soler, Tobias R. Chapman, Louis R. Poisson, Lin of September 27, 2021. Wang, Javier Cote-Sierra, Mark Ryan, Alice McDonald, Sunita Badola, Eric Fedyk, Anthony J. Coyle, Martin R. Hodge and Roland Kolbeck J Immunol 2006; 177:6940-6951; ; doi: 10.4049/jimmunol.177.10.6940 Downloaded from http://www.jimmunol.org/content/177/10/6940 References This article cites 68 articles, 27 of which you can access for free at: http://www.jimmunol.org/content/177/10/6940.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 by guest on September 27, 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 CCR8 Expression Identifies CD4 Memory T Cells Enriched for FOXP3؉ Regulatory and Th2 Effector Lymphocytes Dulce Soler,1 Tobias R. -
231115072.Pdf
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Dartmouth Digital Commons (Dartmouth College) Dartmouth College Dartmouth Digital Commons Open Dartmouth: Faculty Open Access Articles 8-2003 CCR5 Mediates Specific iM gration of Toxoplasma Gondii—Primed CD8+ Lymphocytes to Inflammatory Intestinal Epithelial Cells Souphalone Luangsay Dartmouth College Lloyd H. Kasper Dartmouth College Nicolas Rachinel Dartmouth College Laurie A. Minns Dartmouth College Follow this and additional works at: https://digitalcommons.dartmouth.edu/facoa Part of the Digestive System Diseases Commons, and the Gastroenterology Commons Recommended Citation Luangsay, Souphalone; Kasper, Lloyd H.; Rachinel, Nicolas; and Minns, Laurie A., "CCR5 Mediates Specific iM gration of Toxoplasma Gondii—Primed CD8+ Lymphocytes to Inflammatory Intestinal Epithelial Cells" (2003). Open Dartmouth: Faculty Open Access Articles. 593. https://digitalcommons.dartmouth.edu/facoa/593 This Article is brought to you for free and open access by Dartmouth Digital Commons. It has been accepted for inclusion in Open Dartmouth: Faculty Open Access Articles by an authorized administrator of Dartmouth Digital Commons. For more information, please contact [email protected]. GASTROENTEROLOGY 2003;125:491–500 CCR5 Mediates Specific Migration of Toxoplasma gondii–Primed CD8؉ Lymphocytes to Inflammatory Intestinal Epithelial Cells SOUPHALONE LUANGSAY,* LLOYD H. KASPER,* NICOLAS RACHINEL,* LAURIE A. MINNS,* FRANCK J. D. MENNECHET,* ALAIN -
CCR5 in T Cell-Mediated Liver Diseases: What's Going On? Maureen N
CCR5 in T Cell-Mediated Liver Diseases: What's Going On? Maureen N. Ajuebor, Jillian A. Carey and Mark G. Swain This information is current as J Immunol 2006; 177:2039-2045; ; of September 29, 2021. doi: 10.4049/jimmunol.177.4.2039 http://www.jimmunol.org/content/177/4/2039 Downloaded from References This article cites 62 articles, 20 of which you can access for free at: http://www.jimmunol.org/content/177/4/2039.full#ref-list-1 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 © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. THE JOURNAL OF IMMUNOLOGY BRIEF REVIEWS CCR5 in T Cell-Mediated Liver Diseases: What’s Going On?1 Maureen N. Ajuebor, Jillian A. Carey, and Mark G. Swain2 The chemokine receptor CCR5 came into worldwide Over the past 10 years, chemokines have been the focus of a prominence a decade ago when it was identified as one of great deal of research pertaining to their role in promoting leu- the major coreceptors for HIV infectivity. -
GM-CSF Modulates the Migratory Phenotype of Vaccine-Induced T Cells by Enhancing CXCR3 Expression
GM-CSF modulates the migratory phenotype of vaccine-induced T cells by enhancing CXCR3 expression Il-Kang Na Carmen Scheibenbogen Ulrich Keilholz Department of Hematology, Oncology and Transfusion Medicine, Charité Berlin, Campus Benjamin Franklin, Germany. Background Selective chemokine receptor Inflammatory Local tissue microenvironment CXCR3 Tumor tissue CCR4 Skin CCR9 Tissue specific dendritic cells Small intestine Aim of the study Analysis of • Expression of chemokine receptors CXCR3 and CCR4 on vaccine-induced T cells. • Influence of GM-CSF as vaccine adjuvant on chemokine receptor expression. Materials & Methods • Patient samples: stage III/ IV melanoma 1) Tyrosinase peptide + KLH + GM-CSF 2 cohorts 2) Tyrosinase peptide + KLH • T cell response assessment by IFNγ flow cytometry analysis Phase I trial of tyrosinase peptide with adjuvants GM-CSF and KLH 50 50 40 40 30 30 Tyr specific 20 20 PBMC 6 10 10 / 10 0 0 before P13 P14 P15 P15 P16 P17 P17 P18 P18 P19 P11 P11 P12 P12 P13 P31 P32 P33 P34 P35 P35 P36 P36 P37 P38 P38 P39 P40 # 2 # 4 T cells Tyr + KLH Tyr + KLH + GM-CSF # 6 ng i 250 250 200 200 150 150 KLH specific IFNg-secret 100 100 50 50 0 0 P21 P22 P23 P24 P25 P26 P27 P28 P29 P30 P31 P32 P33 P34 P35 P36 P37 P38 P39 Patient identification Scheibenbogen et al. 2003 CXCR3 expression on KLH-specific T cells no antigen KLH 25.2 0.02 24.7 0.06 74.7 0.04 75.1 0.2 Tyr + KLH cohort CXCR3 46.6 0.02 46.0 0.09 52.1 0.01 51.9 0.06 Tyr + KLH + GM-CSF cohort IFNγ CXCR3, CCR4 and CCR9 expression on KLH-specific T cells with GM-CSF without -
CCR6 IL-17 Express the Chemokine Receptor Human T Cells That Are
Human T Cells That Are Able to Produce IL-17 Express the Chemokine Receptor CCR6 This information is current as Satya P. Singh, Hongwei H. Zhang, John F. Foley, Michael of September 26, 2021. N. Hedrick and Joshua M. Farber J Immunol 2008; 180:214-221; ; doi: 10.4049/jimmunol.180.1.214 http://www.jimmunol.org/content/180/1/214 Downloaded from References This article cites 58 articles, 27 of which you can access for free at: http://www.jimmunol.org/content/180/1/214.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 26, 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 Human T Cells That Are Able to Produce IL-17 Express the Chemokine Receptor CCR61 Satya P. Singh, Hongwei H. Zhang, John F. Foley, Michael N. Hedrick, and Joshua M. Farber2 Some pathways of T cell differentiation are associated with characteristic patterns of chemokine receptor expression. -
Research Article CCR9 Is a Key Regulator of Early Phases of Allergic Airway Inflammation
Hindawi Publishing Corporation Mediators of Inflammation Volume 2016, Article ID 3635809, 16 pages http://dx.doi.org/10.1155/2016/3635809 Research Article CCR9 Is a Key Regulator of Early Phases of Allergic Airway Inflammation C. López-Pacheco,1,2 G. Soldevila,2 G. Du Pont,1,2 R. Hernández-Pando,3 and E. A. García-Zepeda1,2 1 CBRL, Ciudad de Mexico,´ Mexico 2Departamento de Inmunolog´ıa, Instituto de Investigaciones Biomedicas,´ Universidad Nacional Autonoma´ de Mexico,´ 04510 Ciudad de Mexico,´ Mexico 3Departamento de Patolog´ıa Experimental, Instituto Nacional de Ciencias Medicas´ y Nutricion´ “Salvador Zubiran”,´ Tlalpan, 14080 Ciudad de Mexico,´ Mexico Correspondence should be addressed to E. A. Garc´ıa-Zepeda; [email protected] Received 9 May 2016; Accepted 7 August 2016 Academic Editor: Carolina T. Pineiro˜ Copyright © 2016 C. Lopez-Pacheco´ et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Airway inflammation is the most common hallmark of allergic asthma. Chemokine receptors involved in leukocyte recruitment are closely related to the pathology in asthma. CCR9 has been described as a homeostatic and inflammatory chemokine receptor, but its role and that of its ligand CCL25 during lung inflammation remain unknown. To investigate the role of CCR9 as a modulator of airway inflammation, we established an OVA-induced allergic inflammation model in CCR9-deficient mice. Here, we report the expression of CCR9 and CCL25 as early as 6 hours post-OVA challenge in eosinophils and T-lymphocytes. -
Recruitment and Expansion of Tregs Cells in the Tumor Environment—How to Target Them?
cancers Review Recruitment and Expansion of Tregs Cells in the Tumor Environment—How to Target Them? Justine Cinier 1,†, Margaux Hubert 1,†, Laurie Besson 1, Anthony Di Roio 1 ,Céline Rodriguez 1, Vincent Lombardi 2, Christophe Caux 1,‡ and Christine Ménétrier-Caux 1,*,‡ 1 University of Lyon, Claude Bernard Lyon 1 University, INSERM U-1052, CNRS 5286 Centre Léon Bérard, Cancer Research Center of Lyon (CRCL), 69008 Lyon, France; [email protected] (J.C.); [email protected] (M.H.); [email protected] (L.B.); [email protected] (A.D.R.); [email protected] (C.R.); [email protected] (C.C.) 2 Institut de Recherche Servier, 125 Chemin de Ronde, 78290 Croissy-sur-Seine, France; [email protected] * Correspondence: [email protected] † Co-first authorship. ‡ Co-last authorship. Simple Summary: The immune response against cancer is generated by effector T cells, among them cytotoxic CD8+ T cells that destroy cancer cells and helper CD4+ T cells that mediate and support the immune response. This antitumor function of T cells is tightly regulated by a particular subset of CD4+ T cells, named regulatory T cells (Tregs), through different mechanisms. Even if the complete inhibition of Tregs would be extremely harmful due to their tolerogenic role in impeding autoimmune diseases in the periphery, the targeted blockade of their accumulation at tumor sites or their targeted Citation: Cinier, J.; Hubert, M.; depletion represent a major therapeutic challenge. This review focuses on the mechanisms favoring Besson, L.; Di Roio, A.; Rodriguez, C.; Treg recruitment, expansion and stabilization in the tumor microenvironment and the therapeutic Lombardi, V.; Caux, C.; strategies developed to block these mechanisms. -
Colorectal Cancer-Infiltrating T Lymphocytes Display a Distinct
Löfroos et al. Eur J Med Res (2017) 22:40 DOI 10.1186/s40001-017-0283-8 European Journal of Medical Research RESEARCH Open Access Colorectal cancer‑infltrating T lymphocytes display a distinct chemokine receptor expression profle Ann‑Britt Löfroos1,2†, Mohammad Kadivar2†, Sabina Resic Lindehammer1,2 and Jan Marsal1,2,3* Abstract Background: T lymphocytes exert important homeostatic functions in the healthy intestinal mucosa, whereas in case of colorectal cancer (CRC), infltration of T lymphocytes into the tumor is crucial for an efective anti-tumor immune response. In both situations, the recruitment mechanisms of T lymphocytes into the tissues are essential for the immunological functions deciding the outcome. The recruitment of T lymphocytes is largely dependent on their expression of various chemokine receptors. The aim of this study was to identify potential chemokine receptors involved in the recruitment of T lymphocytes to normal human colonic mucosa and to CRC tissue, respectively, by examining the expression of 16 diferent chemokine receptors on T lymphocytes isolated from these tissues. Methods: Tissues were collected from patients undergoing bowel resection for CRC. Lymphocytes were isolated through enzymatic tissue degradation of CRC tissue and nearby located unafected mucosa, respectively. The expres‑ sion of a broad panel of chemokine receptors on the freshly isolated T lymphocytes was examined by fow cytometry. Results: In the normal colonic mucosa, the frequencies of cells expressing CCR2, CCR4, CXCR3, and CXCR6 dif‑ fered signifcantly between CD4+ and CD8+ T lymphocytes, suggesting that the molecular mechanisms mediating T lymphocyte recruitment to the gut difer between CD4+ and CD8+ T lymphocytes. -
The Abnormal Expression of CCR4 and CCR6 on Tregs in Rheumatoid Arthritis
Int J Clin Exp Med 2015;8(9):15043-15053 www.ijcem.com /ISSN:1940-5901/IJCEM0003430 Original Article The abnormal expression of CCR4 and CCR6 on Tregs in rheumatoid arthritis Ning Li1*, Wei Wei2*, Feng Yin3*, Maogen Chen4, Tian R Ma5, Qiang Wu3, Jie R Zhou1, Song-Guo Zheng4,6, Jie Han1 Departments of 1Rheumatology, 3Osteology, Shanghai East Hospital, 6Institute of Immunology, Tongji University School of Medicine, Shanghai, 200120, China; 2Department of Rheumatology, Yuyao People’s Hospital, Yuyao 315400, Zhejiang, China; 4Division of Rheumatology & Immunology, Department of Medicine, Keck School of Medicine of The University of Southern California, Los Angeles 90033, CA, USA; 5Department of Rheumatology, Ningbo Women and Children’s Hospital, Ningbo 315012, Zhejiang, China. *Equal contributors. Received October 28, 2014; Accepted January 7, 2015; Epub September 15, 2015; Published September 30, 2015 Abstract: The study aims to investigate the frequency of CD4+CD25+Foxp3+CD127- T regulatory cells (Tregs) and the expression of CCR4, CCR6 and/or other chemokine receptors on Tregs in peripheral blood (PB) in patients with rheumatoid arthritis, as well as in PB, draining lymph nodes (dLNs), lungs and spleens in collagen-induced arthritis (CIA) mice. We also study the possible role of CCR4 and CCR6 abnormal expression on Tregs in RA pa- tients and the underlying mechanisms. The numbers of Tregs and chemokine receptors expression profile on Tregs in PB from RA patients and healthy controls were investigated by flow cytometry (FACS) using three- or four-color intracellular staining. DBA/1 Foxp3gfp reporter mice were immunized with collagen II (CII) emulsified with CFA. -
Macrophages Confer Survival Signals Via CCR1-Dependent Translational MCL-1 Induction in Chronic Lymphocytic Leukemia
OPEN Oncogene (2017) 36, 3651–3660 www.nature.com/onc ORIGINAL ARTICLE Macrophages confer survival signals via CCR1-dependent translational MCL-1 induction in chronic lymphocytic leukemia MHA van Attekum1,2, S Terpstra1,2, E Slinger1,2, M von Lindern3, PD Moerland4, A Jongejan4, AP Kater1,5,6 and E Eldering2,5,6 Protective interactions with bystander cells in micro-environmental niches, such as lymph nodes (LNs), contribute to survival and therapy resistance of chronic lymphocytic leukemia (CLL) cells. This is caused by a shift in expression of B-cell lymphoma 2 (BCL-2) family members. Pro-survival proteins B-cell lymphoma-extra large (BCL-XL), BCL-2-related protein A1 (BFL-1) and myeloid leukemia cell differentiation protein 1 (MCL-1) are upregulated by LN-residing T cells through CD40L interaction, presumably via nuclear factor (NF)-κB signaling. Macrophages (Mϕs) also reside in the LN, and are assumed to provide important supportive functions for CLL cells. However, if and how Mϕs are able to induce survival is incompletely known. We first established that Mϕs induced survival because of an exclusive upregulation of MCL-1. Next, we investigated the mechanism underlying MCL-1 induction by Mϕs in comparison with CD40L. Genome-wide expression profiling of in vitro Mϕ- and CD40L-stimulated CLL cells indicated activation of the phosphoinositide 3-kinase (PI3K)-V-Akt murine thymoma viral oncogene homolog (AKT)-mammalian target of rapamycin (mTOR) pathway, which was confirmed in ex vivo CLL LN material. Inhibition of PI3K-AKT-mTOR signaling abrogated MCL-1 upregulation and survival by Mϕs, as well as CD40 stimulation. -
Expression and Function of Chemokine Receptors in Human Multiple Myeloma Cmo¨Ller, T Stro¨Mberg, M Juremalm, K Nilsson and G Nilsson
Leukemia (2003) 17, 203–210 2003 Nature Publishing Group All rights reserved 0887-6924/03 $25.00 www.nature.com/leu Expression and function of chemokine receptors in human multiple myeloma CMo¨ller, T Stro¨mberg, M Juremalm, K Nilsson and G Nilsson Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala, Sweden Multiple myeloma (MM) is a B cell tumor characterized by its chemokines, and to their pattern of expression of adhesion selective localization in the bone marrow. The mechanisms that molecules.6 The chemokine receptors implicated in B cell contribute to the multiple myeloma cell recruitment to the bone marrow microenvironment are not well understood. Chemo- migration and proliferation include CXCR4, CXCR5, CCR2, 7–14 kines play a central role for lymphocyte trafficking and homing. CCR6 and CCR7. In this study we have investigated expression and functional The chemokine stromal cell-derived factor-1 (SDF-1) and its importance of chemokine receptors in MM-derived cell lines corresponding receptor CXCR4 have been shown to be essen- and primary MM cells. We found that MM cell lines express tial for bone marrow myelopoiesis and B lymphopoiesis.15,16 functional CCR1, CXCR3 and CXCR4 receptors, and some also SDF-1 is constitutively expressed at high levels by bone mar- CCR6. Although only a minority of the cell lines responded by 17,18 calcium mobilization after agonist stimulation, a migratory row stromal cells. CXCR4 appears to participate in the response to the CCR1 ligands RANTES and MIP-1␣ was regulation of B lymphopoiesis by confining precursors within obtained in 5/6 and 4/6, respectively, of the cell lines tested.