Annotated Gene List HTG Edgeseq Precision Immuno-Oncology Panel
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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 -
Cd160 Mouse Shrna Plasmid (Locus ID 54215) – TR514223 | Origene
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TR514223 Cd160 Mouse shRNA Plasmid (Locus ID 54215) Product data: Product Type: shRNA Plasmids Product Name: Cd160 Mouse shRNA Plasmid (Locus ID 54215) Locus ID: 54215 Synonyms: AU045688; By55 Vector: pRS (TR20003) Format: Retroviral plasmids Components: Cd160 - Mouse, 4 unique 29mer shRNA constructs in retroviral untagged vector(Gene ID = 54215). 5µg purified plasmid DNA per construct Non-effective 29-mer scrambled shRNA cassette in pRS Vector, TR30012, included for free. RefSeq: BC021596, NM_001163496, NM_001163497, NM_018767 Summary: CD160 antigen: Receptor on immune cells capable to deliver stimulatory or inhibitory signals that regulate cell activation and differentiation. Exists as a GPI-anchored and as a transmembrane form, each likely initiating distinct signaling pathways via phosphoinositol 3- kinase in activated NK cells and via LCK and CD247/CD3 zeta chain in activated T cells (By similarity). Receptor for both classical and non-classical MHC class I molecules (PubMed:16177084). Receptor or ligand for TNF superfamily member TNFRSF14, participating in bidirectional cell-cell contact signaling between antigen presenting cells and lymphocytes. Upon ligation of TNFRSF14, provides stimulatory signal to NK cells enhancing IFNG production and anti-tumor immune response (PubMed:25711213). On activated CD4+ T cells, interacts with TNFRSF14 and downregulates CD28 costimulatory signaling, restricting memory and alloantigen-specific immune response (By similarity). In the context of bacterial infection, acts as a ligand for TNFRSF14 on epithelial cells, triggering the production of antimicrobial proteins and proinflammatory cytokines (PubMed:22801499).[UniProtKB/Swiss-Prot Function] shRNA Design: These shRNA constructs were designed against multiple splice variants at this gene locus. -
Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse
Welcome to More Choice CD Marker Handbook For more information, please visit: Human bdbiosciences.com/eu/go/humancdmarkers Mouse bdbiosciences.com/eu/go/mousecdmarkers Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse CD3 CD3 CD (cluster of differentiation) molecules are cell surface markers T Cell CD4 CD4 useful for the identification and characterization of leukocytes. The CD CD8 CD8 nomenclature was developed and is maintained through the HLDA (Human Leukocyte Differentiation Antigens) workshop started in 1982. CD45R/B220 CD19 CD19 The goal is to provide standardization of monoclonal antibodies to B Cell CD20 CD22 (B cell activation marker) human antigens across laboratories. To characterize or “workshop” the antibodies, multiple laboratories carry out blind analyses of antibodies. These results independently validate antibody specificity. CD11c CD11c Dendritic Cell CD123 CD123 While the CD nomenclature has been developed for use with human antigens, it is applied to corresponding mouse antigens as well as antigens from other species. However, the mouse and other species NK Cell CD56 CD335 (NKp46) antibodies are not tested by HLDA. Human CD markers were reviewed by the HLDA. New CD markers Stem Cell/ CD34 CD34 were established at the HLDA9 meeting held in Barcelona in 2010. For Precursor hematopoetic stem cell only hematopoetic stem cell only additional information and CD markers please visit www.hcdm.org. Macrophage/ CD14 CD11b/ Mac-1 Monocyte CD33 Ly-71 (F4/80) CD66b Granulocyte CD66b Gr-1/Ly6G Ly6C CD41 CD41 CD61 (Integrin b3) CD61 Platelet CD9 CD62 CD62P (activated platelets) CD235a CD235a Erythrocyte Ter-119 CD146 MECA-32 CD106 CD146 Endothelial Cell CD31 CD62E (activated endothelial cells) Epithelial Cell CD236 CD326 (EPCAM1) For Research Use Only. -
Dendritic Cell Subsets in Intestinal Immunity and Inflammation Tian Sun, Albert Nguyen and Jennifer L
Dendritic Cell Subsets in Intestinal Immunity and Inflammation Tian Sun, Albert Nguyen and Jennifer L. Gommerman This information is current as J Immunol 2020; 204:1075-1083; ; of September 28, 2021. doi: 10.4049/jimmunol.1900710 http://www.jimmunol.org/content/204/5/1075 Downloaded from References This article cites 152 articles, 56 of which you can access for free at: http://www.jimmunol.org/content/204/5/1075.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 28, 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 © 2020 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Dendritic Cell Subsets in Intestinal Immunity and Inflammation Tian Sun, Albert Nguyen, and Jennifer L. Gommerman The mammalian intestine is a complex environment shaping the ensuing immune response. In this Brief Review,we that is constantly exposed to Ags derived from food, review the different types of classical DC (cDC) located in the microbiota, and metabolites. -
Characterization of FLT3-Itdmut Acute Myeloid Leukemia
Travaglini et al. Blood Cancer Journal (2020) 10:85 https://doi.org/10.1038/s41408-020-00352-9 Blood Cancer Journal ARTICLE Open Access Characterization of FLT3-ITDmut acute myeloid leukemia: molecular profiling of leukemic precursor cells Serena Travaglini1, Daniela Francesca Angelini 2, Valentina Alfonso1, Gisella Guerrera2,SerenaLavorgna1, Mariadomenica Divona1, Anna Maria Nardozza1, Maria Irno Consalvo1, Emiliano Fabiani1,MarcoDeBardi 2, Benedetta Neri3,FabioForghieri4, Francesco Marchesi5, Giovangiacinto Paterno1, Raffaella Cerretti1, Eva Barragan 6, Valentina Fiori7,SabrinaDominici7, Maria Ilaria Del Principe1, Adriano Venditti 1, Luca Battistini2, William Arcese1, Francesco Lo-Coco1, Maria Teresa Voso 1,2 and Tiziana Ottone1,2 Abstract Acute myeloid leukemia (AML) with FLT3-ITD mutations (FLT3-ITDmut) remains a therapeutic challenge, with a still high relapse rate, despite targeted treatment with tyrosine kinase inhibitors. In this disease, the CD34/CD123/CD25/CD99+ leukemic precursor cells (LPCs) phenotype predicts for FLT3-ITD-positivity. The aim of this study was to characterize the distribution of FLT3-ITD mutation in different progenitor cell subsets to shed light on the subclonal architecture of FLT3-ITDmut AML. Using high-speed cell sorting, we sequentially purified LPCs and CD34+ progenitors in samples from patients with FLT3-ITDmut AML (n = 12). A higher FLT3-ITDmut load was observed within CD34/CD123/CD25/CD99+ LPCs, as compared to CD34+ progenitors (CD123+/−,CD25−,CD99low/−)(p = 0.0005) and mononuclear cells (MNCs) (p < 0.0001). This was associated with significantly increased CD99 mean fluorescence intensity in LPCs. 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; Significantly higher FLT3-ITDmut burden was also observed in LPCs of AML patients with a small FLT3-ITDmut clones at diagnosis. -
List of Genes Used in Cell Type Enrichment Analysis
List of genes used in cell type enrichment analysis Metagene Cell type Immunity ADAM28 Activated B cell Adaptive CD180 Activated B cell Adaptive CD79B Activated B cell Adaptive BLK Activated B cell Adaptive CD19 Activated B cell Adaptive MS4A1 Activated B cell Adaptive TNFRSF17 Activated B cell Adaptive IGHM Activated B cell Adaptive GNG7 Activated B cell Adaptive MICAL3 Activated B cell Adaptive SPIB Activated B cell Adaptive HLA-DOB Activated B cell Adaptive IGKC Activated B cell Adaptive PNOC Activated B cell Adaptive FCRL2 Activated B cell Adaptive BACH2 Activated B cell Adaptive CR2 Activated B cell Adaptive TCL1A Activated B cell Adaptive AKNA Activated B cell Adaptive ARHGAP25 Activated B cell Adaptive CCL21 Activated B cell Adaptive CD27 Activated B cell Adaptive CD38 Activated B cell Adaptive CLEC17A Activated B cell Adaptive CLEC9A Activated B cell Adaptive CLECL1 Activated B cell Adaptive AIM2 Activated CD4 T cell Adaptive BIRC3 Activated CD4 T cell Adaptive BRIP1 Activated CD4 T cell Adaptive CCL20 Activated CD4 T cell Adaptive CCL4 Activated CD4 T cell Adaptive CCL5 Activated CD4 T cell Adaptive CCNB1 Activated CD4 T cell Adaptive CCR7 Activated CD4 T cell Adaptive DUSP2 Activated CD4 T cell Adaptive ESCO2 Activated CD4 T cell Adaptive ETS1 Activated CD4 T cell Adaptive EXO1 Activated CD4 T cell Adaptive EXOC6 Activated CD4 T cell Adaptive IARS Activated CD4 T cell Adaptive ITK Activated CD4 T cell Adaptive KIF11 Activated CD4 T cell Adaptive KNTC1 Activated CD4 T cell Adaptive NUF2 Activated CD4 T cell Adaptive PRC1 Activated -
Propranolol-Mediated Attenuation of MMP-9 Excretion in Infants with Hemangiomas
Supplementary Online Content Thaivalappil S, Bauman N, Saieg A, Movius E, Brown KJ, Preciado D. Propranolol-mediated attenuation of MMP-9 excretion in infants with hemangiomas. JAMA Otolaryngol Head Neck Surg. doi:10.1001/jamaoto.2013.4773 eTable. List of All of the Proteins Identified by Proteomics This supplementary material has been provided by the authors to give readers additional information about their work. © 2013 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 eTable. List of All of the Proteins Identified by Proteomics Protein Name Prop 12 mo/4 Pred 12 mo/4 Δ Prop to Pred mo mo Myeloperoxidase OS=Homo sapiens GN=MPO 26.00 143.00 ‐117.00 Lactotransferrin OS=Homo sapiens GN=LTF 114.00 205.50 ‐91.50 Matrix metalloproteinase‐9 OS=Homo sapiens GN=MMP9 5.00 36.00 ‐31.00 Neutrophil elastase OS=Homo sapiens GN=ELANE 24.00 48.00 ‐24.00 Bleomycin hydrolase OS=Homo sapiens GN=BLMH 3.00 25.00 ‐22.00 CAP7_HUMAN Azurocidin OS=Homo sapiens GN=AZU1 PE=1 SV=3 4.00 26.00 ‐22.00 S10A8_HUMAN Protein S100‐A8 OS=Homo sapiens GN=S100A8 PE=1 14.67 30.50 ‐15.83 SV=1 IL1F9_HUMAN Interleukin‐1 family member 9 OS=Homo sapiens 1.00 15.00 ‐14.00 GN=IL1F9 PE=1 SV=1 MUC5B_HUMAN Mucin‐5B OS=Homo sapiens GN=MUC5B PE=1 SV=3 2.00 14.00 ‐12.00 MUC4_HUMAN Mucin‐4 OS=Homo sapiens GN=MUC4 PE=1 SV=3 1.00 12.00 ‐11.00 HRG_HUMAN Histidine‐rich glycoprotein OS=Homo sapiens GN=HRG 1.00 12.00 ‐11.00 PE=1 SV=1 TKT_HUMAN Transketolase OS=Homo sapiens GN=TKT PE=1 SV=3 17.00 28.00 ‐11.00 CATG_HUMAN Cathepsin G OS=Homo -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Dendritic Cell Progenitor Trafficking and Identification and Functional Analyses of Dendritic Cells with Distinct Developmental Origin
Dissertation zum Erwerb des Doctor of Philosophy (Ph.D.) an der Medizinischen Fakultät der Ludwig-Maximilians-Universität zu München Dendritic cell progenitor trafficking and identification and functional analyses of dendritic cells with distinct developmental origin vorgelegt von: Johanna Marie Salvermoser aus: Pfaffenhofen an der Ilm Jahr: 2020 _____________________ First supervisor: Prof. Dr. Barbara Schraml Second supervisor: Prof. Dr. Anne Krug Third supervisor: Prof. Dr. Christian Schulz Fourth supervisor: PD. Dr. rer. nat. Caspar Ohnmacht Dean: Prof. Dr. med. dent. Reinhard Hickel Datum der Verteidigung: 09.03.2020 2 Abstract ABSTRACT Conventional dendritic cells (cDCs), are the major antigen-presenting cell type that bridges the innate and adaptive immune system. DCs are constantly replenished from myeloid bone marrow progenitors which latest stage, pre-cDC, leave the BM, seeds the peripheral tissues and further differentiates into two functionally and developmentally distinct subsets, cDC1 and cDC2. This study aimed to investigate DC development by assessing the trafficking of pre-cDCs and by analyzing the effect of a specific depletion of DC progenitors. The signals that regulate the recruitment of pre-cDCs to different peripheral organs are poorly understood. Therefore, this study aimed to identify pre-cDCs in different peripheral organs and to find differences in expression pattern of trafficking receptors. In this study 39 trafficking receptors have been identified to be expressed on pre-cDCs of the analysed tissues and showed differences in the expression patterns between peripheral organs. These receptors are interesting candidates to further study differences in the recruitment of pre-cDCs to different peripheral tissues This can provide possibilities to influence the recruitment of pre-cDCs in certain diseases, where the replenishment of cDCs is accelerated. -
BD Biosciences New RUO Reagents - November 2020
BD Biosciences New RUO reagents - November 2020 Reactivity Description Format Clone Size Cat. number Hu CD133 FITC W6B3C1 100µg 567029 Hu CD133 FITC W6B3C1 25µg 567033 Hu CD39 PE A1/CD39 100Tst 567156 Hu CD39 PE A1/CD39 25Tst 567157 Hu KIR2DL1/S1/S3/S5 PE HP-MA4 100Tst 567158 Hu KIR2DL1/S1/S3/S5 PE HP-MA4 25Tst 567159 Hu IL-22 Alexa Fluor® 647 MH22B2 100µg 567160 Hu IL-22 Alexa Fluor® 647 MH22B2 25µg 567161 Hu CD99 R718 TU12 50µg 751651 Hu CD161 R718 DX12 50µg 751652 Hu CD116 R718 HGMCSFR-M1 50µg 751653 Hu HLA-G R718 87G 50µg 751670 Hu CD27 R718 O323 50µg 751686 Hu CD80 (B7-1) R718 2D10.4 50µg 751737 Hu Integrin αvβ5 R718 ALULA 50µg 751738 Hu CD266 (Tweak-R) R718 ITEM-4 50µg 751739 Hu ErbB3 (HER-3) R718 SGP1 50µg 751799 Hu TCR Vβ5.1 R718 LC4 50µg 751816 Hu CD123 (IL-3Ra) R718 6H6 50µg 751844 Hu CD1a R718 SK9 50µg 751847 Hu CD20 R718 L27 50µg 751849 Hu Disial GD2 R718 14.G2A 50µg 751851 Reactivity Description Format Clone Size Cat. number Hu CD71 R718 L01.1 50µg 751853 Hu CD278 (ICOS) R718 DX29 50µg 751854 Hu B7-H4 R718 MIH43 50µg 751857 Hu CD53 R718 HI29 50µg 751858 Hu CD197 (CCR7) R718 2-L1-A 50µg 751859 Hu CD197 (CCR7) R718 3D12 50µg 751861 Hu CD31 R718 L133.1 50µg 751863 Hu EGF Receptor R718 EMAB-134 50µg 751864 Hu CD8b R718 2ST8.5H7 50µg 751867 Hu CD31 R718 MBC 78.2 50µg 751869 Hu CD162 R718 KPL-1 50µg 751873 Hu CD24 R718 ML5 50µg 751874 Hu CD159C (NKG2C) R718 134591 50µg 751876 Hu CD169 (Siglec-1) R718 7-239 50µg 751877 Hu CD16b R718 CLB-GRAN11.5 50µg 751880 Hu IgM R718 UCH-B1 50µg 751881 Hu CD275 R718 2D3/B7-H2 50µg 751883 Hu CD307e -
Manipulating Ig Production in Vivo Through CD180 Stimulation Jay
Manipulating Ig production in vivo through CD180 stimulation Jay Wesley Chaplin A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy University of Washington 2012 Reading Committee: Edward A. Clark, Chair Keith B. Elkon Thomas R. Hawn Program authorized to offer degree: Molecular and Cellular Biology University of Washington Abstract Manipulating Ig production in vivo through CD180 stimulation Jay Wesley Chaplin Chair of the Supervisory Committee: Professor Edward A. Clark Department of Immunology CD180 is homologous to TLR4 and regulates TLR4 signaling, yet its function is unclear. This thesis reports that injection of anti-CD180 mAb into mice induced rapid polyclonal IgG, with up to 50-fold increases even in immunodeficient mice. Anti-CD180 rapidly increased transitional B cell number in contrast to anti-CD40 which induced primarily FO B cell and myeloid expansion. Combinations of anti-CD180 with MyD88- dependent TLR ligands biased B cell fate toward synergistic proliferation. Thus, CD180 stimulation induces B cell proliferation and differentiation, causing rapid increases in IgG, and integrates MyD88-dependent TLR signals to regulate proliferation and differentiation. This thesis also reports that targeting Ag to CD180 rapidly induces Ag-specific IgG. IgG responses were robust, diverse, and partially T cell-independent, as both CD40- and T cell deficient mice responded after CD180 targeting. IgG production occurred with either hapten- or OVA-conjugated anti-CD180, and was specific for Ag coupled to anti- CD180. Simultaneous BCR and CD180 stimulation enhanced activation compared to either stimulus alone. Adoptive transfer experiments demonstrated that CD180 expression was required on B cells but not on DCs for Ab induction. -
Targeting Dendritic Cells with Antigen-Delivering Antibodies for Amelioration of Autoimmunity in Animal Models of Multiple Sclerosis and Other Autoimmune Diseases
antibodies Review Targeting Dendritic Cells with Antigen-Delivering Antibodies for Amelioration of Autoimmunity in Animal Models of Multiple Sclerosis and Other Autoimmune Diseases Courtney A. Iberg and Daniel Hawiger * Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, Doisy Research Center, 1205 Carr Lane, St. Louis, MO 63104, USA; [email protected] * Correspondence: [email protected] Received: 31 March 2020; Accepted: 30 April 2020; Published: 15 June 2020 Abstract: The specific targeting of dendritic cells (DCs) using antigen-delivering antibodies has been established to be a highly efficient protocol for the induction of tolerance and protection from autoimmune processes in experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), as well as in some other animal disease models. As the specific mechanisms of such induced tolerance are being investigated, the newly gained insights may also possibly help to design effective treatments for patients. Here we review approaches applied for the amelioration of autoimmunity in animal models based on antibody-mediated targeting of self-antigens to DCs. Further, we discuss relevant mechanisms of immunological tolerance that underlie such approaches, and we also offer some future perspectives for the application of similar methods in certain related disease settings such as transplantation. Keywords: dendritic cells; tolerance; antigen targeting; chimeric antibodies; autoimmunity; multiple sclerosis; diabetes 1. Introduction Over one hundred years ago, Paul Ehrlich coined the term “horror autotoxicus” to define an immune attack against an organism’s healthy tissues [1]. Since then, our knowledge of the complex mechanisms of the immune system as well as our understanding of the pathogenesis of specific autoimmune diseases have grown tremendously.