Longitudinal Immunological Characterization of the First Presensitized Recipient of a Face Transplant
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ENSG Gene Encodes Effector TCR Pathway Costimulation Inhibitory/Exhaustion Synapse/Adhesion Chemokines/Receptors
ENSG Gene Encodes Effector TCR pathway Costimulation Inhibitory/exhaustion Synapse/adhesion Chemokines/receptors ENSG00000111537 IFNG IFNg x ENSG00000109471 IL2 IL-2 x ENSG00000232810 TNF TNFa x ENSG00000271503 CCL5 CCL5 x x ENSG00000139187 KLRG1 Klrg1 x ENSG00000117560 FASLG Fas ligand x ENSG00000121858 TNFSF10 TRAIL x ENSG00000134545 KLRC1 Klrc1 / NKG2A x ENSG00000213809 KLRK1 Klrk1 / NKG2D x ENSG00000188389 PDCD1 PD-1 x x ENSG00000117281 CD160 CD160 x x ENSG00000134460 IL2RA IL-2 receptor x subunit alpha ENSG00000110324 IL10RA IL-10 receptor x subunit alpha ENSG00000115604 IL18R1 IL-18 receptor 1 x ENSG00000115607 IL18RAP IL-18 receptor x accessory protein ENSG00000081985 IL12RB2 IL-12 receptor x beta 2 ENSG00000186810 CXCR3 CXCR3 x x ENSG00000005844 ITGAL CD11a x ENSG00000160255 ITGB2 CD18; Integrin x x beta-2 ENSG00000156886 ITGAD CD11d x ENSG00000140678 ITGAX; CD11c x x Integrin alpha-X ENSG00000115232 ITGA4 CD49d; Integrin x x alpha-4 ENSG00000169896 ITGAM CD11b; Integrin x x alpha-M ENSG00000138378 STAT4 Stat4 x ENSG00000115415 STAT1 Stat1 x ENSG00000170581 STAT2 Stat2 x ENSG00000126561 STAT5a Stat5a x ENSG00000162434 JAK1 Jak1 x ENSG00000100453 GZMB Granzyme B x ENSG00000145649 GZMA Granzyme A x ENSG00000180644 PRF1 Perforin 1 x ENSG00000115523 GNLY Granulysin x ENSG00000100450 GZMH Granzyme H x ENSG00000113088 GZMK Granzyme K x ENSG00000057657 PRDM1 Blimp-1 x ENSG00000073861 TBX21 T-bet x ENSG00000115738 ID2 ID2 x ENSG00000176083 ZNF683 Hobit x ENSG00000137265 IRF4 Interferon x regulatory factor 4 ENSG00000140968 IRF8 Interferon -
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. -
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. -
Transplant Immunology.Pdf
POLICY BRIEFING Transplant Immunology September 2017 The British Society of Immunology is the largest Introduction immunology society in Europe. Our mission is to promote excellence in immunological research, scholarship and Transplantation is the process of moving cells, tissues, or clinical practice in order to improve human and animal organs, from one site to another, either within the same health. We represent the interests of more than 3,000 person or between a donor and a recipient. If an organ immunologists working in academia, clinical medicine, system fails, or becomes damaged as a consequence of and industry. We have strong international links and disease or injury, it can be replaced with a healthy organ collaborate with our European, American and Asian or tissue from a donor. partner societies in order to achieve our aims. Organ transplantation is a major operation and is only Key points: offered when all other treatment options have failed. Consequently, it is often a life-saving intervention. In • Transplantation is the process of moving cells, 2015/16, 4,601 patient lives were saved or improved in i tissues or organs from one site to another for the the UK by an organ transplant. Kidney transplants are purpose of replacing or repairing damaged or the most common organ transplanted on the NHS in diseased organs and tissues. It saves thousands the UK (3,265 in 2015/16), followed by the liver (925), and i of lives each year. However, the immune system pancreas (230). In addition, a total of 383 combined heart poses a significant barrier to successful organ and lung transplants were performed, while in 2015/16. -
Complementary DNA Microarray Analysis of Chemokines and Their Receptors in Allergic Rhinitis RX Zhang,1 SQ Yu,2 JZ Jiang,3 GJ Liu3
RX Zhang, et al ORIGINAL ARTICLE Complementary DNA Microarray Analysis of Chemokines and Their Receptors in Allergic Rhinitis RX Zhang,1 SQ Yu,2 JZ Jiang,3 GJ Liu3 1 Department of Otolaryngology, Huadong Hospital, Fudan University, Shanghai, China 2 Department of Otolaryngology , Jinan General Hospital of PLA, Shandong, China 3 Department of Otolaryngology, Changhai Hospital, Second Military Medical University, Shanghai, China ■ Abstract Objective: To analyze the roles of chemokines and their receptors in the pathogenesis of allergic rhinitis by observing the complementary DNA (cDNA) expression of the chemokines and their receptors in the nasal mucosa of patients with and without allergic rhinitis, using gene chips. Methods: The total RNAs were isolated from the nasal mucosa of 20 allergic rhinitis patients and purifi ed to messenger RNAs, and then reversely transcribed to cDNAs and incorporated with samples of fl uorescence-labeled with Cy5-dUPT (rhinitis patient samples) or Cy3- dUTP (control samples of nonallergic nasal mucosa). Thirty-nine cDNAs of chemokines and their receptors were latticed into expression profi le chips, which were hybridized with probes and then scanned with the computer to study gene expression according to the different fl uorescence intensities. Results: The cDNAs of the following chemokines were upregulated: CCL1, CCL2, CCL5, CCL7, CCL8, CCL11, CCL13, CCL14, CCL17, CCL18, CCL19, CCL24, and CX3CL1 in most of the allergic rhinitis sample chips. CCR2, CCR3, CCR4, CCR5, CCR8 and CX3CR1 were the highly expressed receptor genes. Low expression of CXCL4 was found in these tissues. Conclusion: The T helper cell (TH) immune system is not well regulated in allergic rhinitis. -
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. -
Anti-CCL13 / MCP4 Antibody (Biotin) (ARG65993)
Product datasheet [email protected] ARG65993 Package: 50 μg anti-CCL13 / MCP4 antibody (Biotin) Store at: 4°C Summary Product Description Biotin-conjugated Goat Polyclonal antibody recognizes CCL13 / MCP4 Tested Reactivity Hu Tested Application ELISA, WB Host Goat Clonality Polyclonal Isotype IgG Target Name CCL13 / MCP4 Antigen Species Human Immunogen E. coli derived recombinant Human CCL13 / MCP4. (QPDALNVPST CCFTFSSKKI SLQRLKSYVI TTSRCPQKAV IFRTKLGKEI CADPKEKWVQ NYMKHLGRKA HTLKT) Conjugation Biotin Alternate Names SCYA13; C-C motif chemokine 13; Monocyte chemotactic protein 4; Small-inducible cytokine A13; CKb10; SCYL1; Monocyte chemoattractant protein 4; MCP-4; NCC-1; NCC1; CK-beta-10 Application Instructions Application table Application Dilution ELISA Direct: 0.25 - 1.0 µg/ml Sandwich: 0.25 - 1.0 µg/ml with ARG65992 as a capture antibody WB 0.1 - 0.2 µg/ml Application Note * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist. Calculated Mw 11 kDa Properties Form Liquid Purification Purified by affinity chromatography. Buffer PBS (pH 7.2) Concentration 1 mg/ml Storage instruction Aliquot and store in the dark at 2-8°C. Keep protected from prolonged exposure to light. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use. Note For laboratory research only, not for drug, diagnostic or other use. www.arigobio.com 1/2 Bioinformation Database links GeneID: 6357 Human Swiss-port # Q99616 Human Gene Symbol CCL13 Gene Full Name chemokine (C-C motif) ligand 13 Background This antimicrobial gene is one of several Cys-Cys (CC) cytokine genes clustered on the q-arm of chromosome 17. -
9. Types of Rejection Table of Contents 9.1 Antibody-Mediated Rejection
9. Types of rejection Table of Contents 9.1 Antibody-mediated rejection 9.2 Chronic rejection 9.3 Hyperacute rejection 9.4 T-cell mediated rejection 9.5 Donor specific cell free DNA marker 9.1 Antibody-mediated rejection The 2019 Expert Consensus from the Transplantation Society Working Group (2020). Recommended Treatment for Antibody-mediated Rejection after Kidney Transplantation. Transplantation. 2020 Jan 8. doi: 10.1097/TP.0000000000003095. [Epub ahead of print]. Retrieved from: https://www.ncbi.nlm.nih.gov/pubmed/31895348 • A consensus of expert opinion in regards to standard of care treatment for active and chronic active AMR after kidney transplantation Yamanashi K, Chen-Yoshikawa TF, Hamaji M, et al (2020). Outcomes of combination therapy including rituximab for antibody-mediated rejection after lung transplantation. Gen Thorac Cardiovasc Surg. 2020;68(2):142–149. doi:10.1007/s11748-019-01189-1. Retrieved from: https://europepmc.org/article/med/31435872 • This study is a retrospective analysis of a single center’s experience of using combination therapy (methylprednisolone, plasma exchange, and IVIG) including rituximab for post lung transplant AMR in Japanese patients. Spica D, Junker T, Dickenmann M, et al (2019). Daratumumab for Treatment of Antibody-Mediated Rejection after ABO-Incompatible Kidney Transplantation. Case Rep Nephrol Dial. 2019;9(3):149–157. Published 2019 Nov 13. doi:10.1159/000503951. Retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6902247/ • A case report detailing the use of Daratnumumab for treatment of therapy-refractory AMR in the context of ABO-incompatible kidney transplantation. Kincaide E, Hitchman K, Hall R, Yamaguchi I, Ding Y, Crowther B (2019). -
Chronic Rejection Autoimmunity
Antibodies to MHC Class I Induce Autoimmunity: Role in the Pathogenesis of Chronic Rejection This information is current as Naohiko Fukami, Sabarinathan Ramachandran, Deepti Saini, of September 26, 2021. Michael Walter, William Chapman, G. Alexander Patterson and Thalachallour Mohanakumar J Immunol 2009; 182:309-318; ; doi: 10.4049/jimmunol.182.1.309 http://www.jimmunol.org/content/182/1/309 Downloaded from References This article cites 54 articles, 10 of which you can access for free at: http://www.jimmunol.org/content/182/1/309.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 © 2009 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Antibodies to MHC Class I Induce Autoimmunity: Role in the Pathogenesis of Chronic Rejection1 Naohiko Fukami,* Sabarinathan Ramachandran,* Deepti Saini,* Michael Walter,‡ William Chapman,* G. Alexander Patterson,§ and Thalachallour Mohanakumar2*† Alloimmunity to mismatched donor HLA-Ags and autoimmunity to self-Ags have been hypothesized to play an important role in immunopathogenesis of chronic rejection of transplanted organs. -
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). -
Chemochine E Immunità
Chemochine e Immunità Mariagrazia Uguccioni AIBT 2016 – Pesaro 1987 – Discovery of the first “chemotactic cytokine” – IL8 Marco Baggiolini Theodor Kocher Institute University of Bern (CH) The Chemokine System - 2016 CCL23 CXCL8 CCL15 CXCL7 CCL14 CXCL6 CCL13 CXCL5 CXCL8 CXCL3 CCL8 CXCL6 CCL7 CXCL11 CXCL2 CXCL1 CCL5 CCL13 CXCL10 CCL3 CCL8 CXCR1 CXCL9 CCL7 CCL26 CXCR2 CCR1 CCL2 CCL13 CXCR3 CCL11 CXCL12 CCR2 CCL8 CCL7 CXCR4 CCL5 CCR3 CXCL13 CXCR5 CCL22 CCL17 CCR4 CXCL16 CXCR6 CCL3 CCR5 CCL4 CXCL17 CXCR8 CCL5 CCL8 CCR6 CX3CR1 CCL20 CX3CL1 XCR1 CCR7 XCL1 CCL19 CCR10 CCR8 XCL2 CCR9 CCL21 CCL27 CCL1 CCL28 CCL25 Cell Migration Selectin-mediated rolling 1 Chemoattractan signalling 2 Integrin-mediated cell adhesion 3 Step 1: attachement and rolling Migration along Step 2: activation chemotactic gradient Step 3: arrest and adhesion Chemokine source Functional Modules in Cell Migration T naive IL-2 CCR7 mature DC Priming B naive IL-6 CXCR5 FDC, TFH Antibody immature DC GM-CSF CCR1, CCR5 T naive Antigen uptake TH1 IFN- CCR5 M Bacteria TH2 IL-4, IL-5 CCR3 Eos/Bas Parasites TH17 IL-17, IL-22 CCR6 Neut Fungi CTL IFN-, Perf CXCR3 M Virus From Blood to Tissue CCR1 Tissue Blood CCR2 CCR2 CCR5 CXCR3 From Tissue to Lymph Nodes CCL21 Lymph nodes are privileged sites normal for dendritic cell-naïve T cell encounters CCL21 CCR7 CCL21 inflamed CCL19 from S. Lira, Nat Immunol 2005, 6:866. Functional Modules in Cell Migration T naive IL-2 CCR7 mature DC Priming B naive IL-6 CXCR5 FDC, TFH Antibody immature DC GM-CSF CCR1, CCR5 T naive Antigen uptake TH1 IFN- CCR5 -
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.