DOCSLIB.ORG

IMMUNOLOGY 2019™ Program

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
IMMUNOLOGY 2019™ Program Scientific Program Book IMMUNOLOGY 2019™ The Annual Meeting of the American Association of Immunologists May 9–13, 2019 San Diego Convention Center San Diego, California TABLE OF CONTENTS Thursday Afternoon Sessions .......................................................................................... 1 Friday Morning Sessions .................................................................................................. 7 Friday Afternoon Sessions ............................................................................................... 13 Friday Posters ...................................................................................................................19 Saturday Morning Sessions ............................................................................................. 43 Saturday Afternoon Sessions ........................................................................................... 50 Saturday Posters .............................................................................................................. 56 Sunday Morning Sessions ............................................................................................... 82 Sunday Afternoon Sessions ............................................................................................. 88 Sunday Posters ................................................................................................................ 94 Monday Morning Sessions ............................................................................................... 121 Speaker Disclosures ......................................................................................................... 127 Author/Speaker Index ....................................................................................................... 133 THURSDAY—PM THURSDAY AFTERNOON MAY 9 T 1. MAST CELLS: PHENOTYPE TO FUNCTION 12:30 Human natural regulatory T cells recognize peptides of H the heavy constant region of immunoglobulins Block Symposium U presented by IgG+ B cells. L-E. Hsieh, J. Sidney, THU. 12:15 PM—ROOM 26AB N. Behnamfar, J.C. Burns, D. Boyle, G.S. Firestein, A. Sette and A. Franco. Sch. of Med., Univ. of CHAIRS: T. SUMPTER, T. KAWAKAMI California, San Diego and La Jolla Inst. for 12:15 Comprehensive characterization of the mast cell Immunology. (57.4) surface proteome. N.J. Shubin, K. Niino, 12:45 CD71+erythroid cells promote Tregs and via V. Kasprzak, R. James and A.M. Piliponsky. ectonucleotides CD39 and CD73 modulate T cell Seattle Children’s Res. Inst. (54.1) responses. S. Elahi, S. Shahbaz and P. Koleva. 12:30 Early life adversity programs mast cells toward a Univ. of Alberta, Canada. (57.5) hyperactive phenotype into adulthood. 1:00 Negative feedback control of autoimmunity by a novel N.C. Maradiaga, C. Pohl, E. Mackey and population of regulatory unconventional CD8+ T cells. A.J. Moeser. Michigan State Univ. (54.2) I. Marrero, H. Sheng, I. Maricic, S.S. Fanchiang, 12:45 Perinatal androgens drive sex differences in mast cell S. Zhang, D. Sant’Angelo and V. Kumar. Univ. of phenotype and severity of mast cell disease. California, San Diego and Rutgers Univ. (57.10) E. Mackey and A.J. Moeser. Michigan State Univ. 1:15 A wave of Foxp3+ regulatory T cell accumulation in (54.15) neonatal liver plays unique roles in maintaining 1:00 Skin microbiome regulates SCF level in Keratinocytes self-tolerance. Q. Ge and M. Li. Peking Univ., and defines mast cell maturation. C-C. Wu, Z. Wang China. (57.14) and A. Di Nardo. Univ. of California, San Diego. 1:30 LAG-3+-induced regulatory T cells confer infectious (54.16) tolerance with suppression of IFN-g response 1:15 Allergen-induced disulfide-linked dimers/oligomers of decoupled from reserved proliferation. C-T. Huang, histamine-releasing factor enhance mast cell A. Dutta, C-Y. Hung, T-C. Chen, C-Y. Lin, Y-C. Lin, activation. Y. Kawakami, K. Kasakura, T. Ando, C-S. Chang, T-A. Chen and Y-L. Huang. Chang Y. Kawakami and T. Kawakami. La Jolla Inst. for Gung Mem. Hosp., Taiwan. (57.16) Immunology and Atopy (Allergy) Res. Ctr., Juntendo 1:45 c-Maf-dependent Treg cell control of intestinal TH17 Univ. Grad. Sch. of Med., Japan. (54.4) cells and IgA establishes host-microbiota 1:30 Selective serotonin reuptake inhibitors suppress mast homeostasis. S. Rutz, C. Neumann, J. Blume, cell function. T. Haque and J. Ryan. Virginia A. Kalies and A. Scheffold. Genentech, Inc., Commonwealth Univ. (54.11) German Rheumatism Res. Ctr., Germany, The 1:45 STAT5b dimers and tetramers are critical for mast cell Walter and Eliza Hall Inst. of Med. Res. and function. K.N. Kiwanuka, J. Lin, W.J. Leonard and Christian Albrechts Univ., Germany. (57.19) J.J. Ryan. Virginia Commonwealth Univ. and NHLBI, 2:00 Recently alloactivated CD4+CD8-CD25+T regulatory NIH, MD. (54.13) cells express CD8alpha and are potent suppressor 2:00 Ceramide-CD300f interaction inhibits Mrgprb2- cells. B.M. Hall, N.D. Verma, C.M. Robinson, mediated mast cell activation and pseudo-allergic C. Wang, A. Sharland, G. Tran, P. Wilcox and drug reactions in mice. A. Takamori, T. Ando, S.J. Hodgkinson. Univ. of New South Wales, A. Kaitani, A. Maehara, K. Izawa, K. Okumura Australia and Sydney Univ., Australia. (57.20) and J. Kitaura. Juntendo Univ. Graduate Sch. of Med., Japan. (54.8) 3. MYELOID CELLS Block Symposium 2. TREGS AND TH17 THU. 12:15 PM—ROOM 31ABC Block Symposium CHAIRS: R.G. SCHERAGA, M. MESSMER THU. 12:15 PM—ROOM 30CDE 12:15 Myeloid responders to programmed cell death. CHAIRS: A. FRANCO, V. KUMAR M.N. Messmer, A.G. Snyder, M.Y. Gerner and 12:15 Phenotypic and functional characterisation of expanded A. Oberst. Univ. of Washington. (58.2) antigen-specific regulatory T cells towards clinical 12:30 TRPV4 mediates the macrophage phagocytic and translation. J. Bianchi, R.I. Azevedo, A.I.S. Vieira, cytokine response to leptin. R.G. Scheraga, D. Ligeiro, C.L. da Silva and J.F. de Lacerda. IMM, A. Perelas, S. Abraham, L. Grove, B.D. Southern, FMUL, CF, Lisbon, Spain, CSTL, IPST-IP, Spain and J. Crish and M. Olman. Cleveland Clin. (58.4) IST-iBB. (57.2) 1 THURSDAY—PM 12:45 Creatine shapes macrophage polarization by 1:15 TRAF3IP3 negatively regulates type I interferon reprogramming L-arginine metabolism. L. Ji, signaling by suppressing TBK1. M. Deng, X. Zhao, B. Zhang, L. Kang, W. Song, B. Zhao, J.W. Tam, H. Guo, L. Zhang, B.K. Davis, W. Xie, L. Chen and X. Hu. Inst. for Immunology and J. Brickey, S. Sun and J.P. Ting. Lineberger Sch. of Med., Tsinghua Univ., China, Sch. of Comprehensive Cancer Ctr., Univ. of North Pharmaceutical Sci., Tsinghua Univ., China, Carolina, Chapel Hill, Dept. of Biol., Franklin and Hospital for Special Surgery Res. Div. and the Marshall Col., Lancaster, PA and Univ. of Texas David Z. Rosensweig Genomics Ctr. and Tsinghua- MD Anderson Cancer Ctr. (64.12) Peking Center for Life Sci., School of Life Sci., 1:30 Induction of innate antiviral immunity through a novel Tsinghua Univ., China. (58.5) pattern recognition receptor, the RNA helicase 1:00 WITHDRAWN DHX16, is regulated by unanchored K48-linked 1:15 Itaconate inhibits alternative activation of macrophages poly-ubiquitin chains. A. Hage, P. Bharaj and by targeting Janus kinase 1. M.C. Runtsch and R. Rajsbaum. Univ. of Texas Med. Br. (64.16) L. O’Neill. Trinity Col. Dublin, Ireland. (58.11) 1:45 NME4 regulates TLR3 activation and type I IFN 1:30 IL-34 differentiation of immunosuppressive production through autophagy-dependent TRAF6 macrophage. K. Kelly-Scumpia, R. Shirazi and degradation. B. Sun, X.H. Zhao and R.H. Zhang. R. Modlin. Univ. of California, Los Angeles. (58.13) Shanghai Inst. of Biochemistry and Cell Biol., 1:45 Sympathetic nervous tone influences anti-tumor Chinese Acad. of Sci., China. (64.22) immunity by mediating accumulation of myeloid- 2:00 Dysregulated CARD9 signaling in neutrophils drives derived suppressor cells and regulatory T-cells. inflammation in a mouse model of neutrophilic J.T. Nevin, W.L. Corwin and P.K. Srivastava. dermatoses. S. Tartey and T-D. Kanneganti. St. Univ. of Connecticut Hlth. Ctr. (58.15) Jude Children’s Res. Hosp. (64.25) 2:00 Fatty acid transporter 2 regulates the suppressive functions of PMN-MDSC in cancer. F. Veglia, 5. CYTOKINE AND T CELL-BASED V. Tyurin, M. Blasi, A. De Leo, L. Donthireddy, IMMUNOTHERAPY C. DiRusso, P. Black, V. Kagan and D.I. Gabrilovich. The Wistar Inst., Univ. of Block Symposium Pittsburgh, Duke Univ. and Univ. of Nebraska- THU. 12:15 PM—ROOM 29ABCD Lincoln. (58.18) CHAIRS: M. KROGSGAARD, C. WARE 4. INNATE IMMUNE SENSING AND SIGNALING 12:15 A powerful ICOS agonist that enhances anti-tumor Block Symposium immune responses restored by immune checkpoint inhibitors. J. Gariepy, A. Prodeus, A. Sparkes, THU. 12:15 PM—ROOM 25ABC N. Fischer and S. Saha. Sunnybrook Res. Inst., Canada, Univ. of Toronto, Canada and McMaster CHAIRS: K. KOBAYASHI, E. AMIEL Univ., Canada. (71.5) 12:15 Role of NLRC5 and IRF1 in the induction of MHC class I. 12:30 A novel agonist of CD137 immune checkpoint stimulator S. Vijayan, T.B. Meissner, K-H. Lee, Y-J. Liu, serves as a cancer immunoprevention agent with I. Downs, T. Sidiq, C. Zhang, P.J. van den Elsen efficacy against various tumor types. L. Batra, and K.S. Kobayashi. Texas A&M Hlth. Sci. Ctr., H.B. Barsoumian, P. Shrestha, J.L. Hawthorne, Harvard Med. Sch. and Leiden Univ. Med. Ctr., W.S. Bowen, H. Zhao, N.K. Egilmez, The Netherlands. (64.20) J.G. Gomez-Gutierrez, H. Shirwan and 12:30 Syk-dependent glycolytic reprogramming in dendritic E.S. Yolcu. Inst. for Cellular Therapeutics, cells regulates IL-1-beta production
Load more

Recommended publications
  • Environmental Influences on Endothelial Gene Expression
    ENDOTHELIAL CELL GENE EXPRESSION John Matthew Jeff Herbert Supervisors: Prof. Roy Bicknell and Dr. Victoria Heath PhD thesis University of Birmingham August 2012 University of Birmingham Research Archive e-theses repository This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. ABSTRACT Tumour angiogenesis is a vital process in the pathology of tumour development and metastasis. Targeting markers of tumour endothelium provide a means of targeted destruction of a tumours oxygen and nutrient supply via destruction of tumour vasculature, which in turn ultimately leads to beneficial consequences to patients. Although current anti -angiogenic and vascular targeting strategies help patients, more potently in combination with chemo therapy, there is still a need for more tumour endothelial marker discoveries as current treatments have cardiovascular and other side effects. For the first time, the analyses of in-vivo biotinylation of an embryonic system is performed to obtain putative vascular targets. Also for the first time, deep sequencing is applied to freshly isolated tumour and normal endothelial cells from lung, colon and bladder tissues for the identification of pan-vascular-targets. Integration of the proteomic, deep sequencing, public cDNA libraries and microarrays, delivers 5,892 putative vascular targets to the science community.
    [Show full text]
  • Transcriptional Control of Tissue-Resident Memory T Cell Generation
    Transcriptional control of tissue-resident memory T cell generation Filip Cvetkovski Submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Graduate School of Arts and Sciences COLUMBIA UNIVERSITY 2019 © 2019 Filip Cvetkovski All rights reserved ABSTRACT Transcriptional control of tissue-resident memory T cell generation Filip Cvetkovski Tissue-resident memory T cells (TRM) are a non-circulating subset of memory that are maintained at sites of pathogen entry and mediate optimal protection against reinfection. Lung TRM can be generated in response to respiratory infection or vaccination, however, the molecular pathways involved in CD4+TRM establishment have not been defined. Here, we performed transcriptional profiling of influenza-specific lung CD4+TRM following influenza infection to identify pathways implicated in CD4+TRM generation and homeostasis. Lung CD4+TRM displayed a unique transcriptional profile distinct from spleen memory, including up-regulation of a gene network induced by the transcription factor IRF4, a known regulator of effector T cell differentiation. In addition, the gene expression profile of lung CD4+TRM was enriched in gene sets previously described in tissue-resident regulatory T cells. Up-regulation of immunomodulatory molecules such as CTLA-4, PD-1, and ICOS, suggested a potential regulatory role for CD4+TRM in tissues. Using loss-of-function genetic experiments in mice, we demonstrate that IRF4 is required for the generation of lung-localized pathogen-specific effector CD4+T cells during acute influenza infection. Influenza-specific IRF4−/− T cells failed to fully express CD44, and maintained high levels of CD62L compared to wild type, suggesting a defect in complete differentiation into lung-tropic effector T cells.
    [Show full text]
  • Single-Cell RNA Sequencing Demonstrates the Molecular and Cellular Reprogramming of Metastatic Lung Adenocarcinoma
    ARTICLE https://doi.org/10.1038/s41467-020-16164-1 OPEN Single-cell RNA sequencing demonstrates the molecular and cellular reprogramming of metastatic lung adenocarcinoma Nayoung Kim 1,2,3,13, Hong Kwan Kim4,13, Kyungjong Lee 5,13, Yourae Hong 1,6, Jong Ho Cho4, Jung Won Choi7, Jung-Il Lee7, Yeon-Lim Suh8,BoMiKu9, Hye Hyeon Eum 1,2,3, Soyean Choi 1, Yoon-La Choi6,10,11, Je-Gun Joung1, Woong-Yang Park 1,2,6, Hyun Ae Jung12, Jong-Mu Sun12, Se-Hoon Lee12, ✉ ✉ Jin Seok Ahn12, Keunchil Park12, Myung-Ju Ahn 12 & Hae-Ock Lee 1,2,3,6 1234567890():,; Advanced metastatic cancer poses utmost clinical challenges and may present molecular and cellular features distinct from an early-stage cancer. Herein, we present single-cell tran- scriptome profiling of metastatic lung adenocarcinoma, the most prevalent histological lung cancer type diagnosed at stage IV in over 40% of all cases. From 208,506 cells populating the normal tissues or early to metastatic stage cancer in 44 patients, we identify a cancer cell subtype deviating from the normal differentiation trajectory and dominating the metastatic stage. In all stages, the stromal and immune cell dynamics reveal ontological and functional changes that create a pro-tumoral and immunosuppressive microenvironment. Normal resident myeloid cell populations are gradually replaced with monocyte-derived macrophages and dendritic cells, along with T-cell exhaustion. This extensive single-cell analysis enhances our understanding of molecular and cellular dynamics in metastatic lung cancer and reveals potential diagnostic and therapeutic targets in cancer-microenvironment interactions. 1 Samsung Genome Institute, Samsung Medical Center, Seoul 06351, Korea.
    [Show full text]
  • Supplementary Table S5. Differentially Expressed Gene Lists of PD-1High CD39+ CD8 Tils According to 4-1BB Expression Compared to PD-1+ CD39- CD8 Tils
    BMJ Publishing Group Limited (BMJ) disclaims all liability and responsibility arising from any reliance Supplemental material placed on this supplemental material which has been supplied by the author(s) J Immunother Cancer Supplementary Table S5. Differentially expressed gene lists of PD-1high CD39+ CD8 TILs according to 4-1BB expression compared to PD-1+ CD39- CD8 TILs Up- or down- regulated genes in Up- or down- regulated genes Up- or down- regulated genes only PD-1high CD39+ CD8 TILs only in 4-1BBneg PD-1high CD39+ in 4-1BBpos PD-1high CD39+ CD8 compared to PD-1+ CD39- CD8 CD8 TILs compared to PD-1+ TILs compared to PD-1+ CD39- TILs CD39- CD8 TILs CD8 TILs IL7R KLRG1 TNFSF4 ENTPD1 DHRS3 LEF1 ITGA5 MKI67 PZP KLF3 RYR2 SIK1B ANK3 LYST PPP1R3B ETV1 ADAM28 H2AC13 CCR7 GFOD1 RASGRP2 ITGAX MAST4 RAD51AP1 MYO1E CLCF1 NEBL S1PR5 VCL MPP7 MS4A6A PHLDB1 GFPT2 TNF RPL3 SPRY4 VCAM1 B4GALT5 TIPARP TNS3 PDCD1 POLQ AKAP5 IL6ST LY9 PLXND1 PLEKHA1 NEU1 DGKH SPRY2 PLEKHG3 IKZF4 MTX3 PARK7 ATP8B4 SYT11 PTGER4 SORL1 RAB11FIP5 BRCA1 MAP4K3 NCR1 CCR4 S1PR1 PDE8A IFIT2 EPHA4 ARHGEF12 PAICS PELI2 LAT2 GPRASP1 TTN RPLP0 IL4I1 AUTS2 RPS3 CDCA3 NHS LONRF2 CDC42EP3 SLCO3A1 RRM2 ADAMTSL4 INPP5F ARHGAP31 ESCO2 ADRB2 CSF1 WDHD1 GOLIM4 CDK5RAP1 CD69 GLUL HJURP SHC4 GNLY TTC9 HELLS DPP4 IL23A PITPNC1 TOX ARHGEF9 EXO1 SLC4A4 CKAP4 CARMIL3 NHSL2 DZIP3 GINS1 FUT8 UBASH3B CDCA5 PDE7B SOGA1 CDC45 NR3C2 TRIB1 KIF14 TRAF5 LIMS1 PPP1R2C TNFRSF9 KLRC2 POLA1 CD80 ATP10D CDCA8 SETD7 IER2 PATL2 CCDC141 CD84 HSPA6 CYB561 MPHOSPH9 CLSPN KLRC1 PTMS SCML4 ZBTB10 CCL3 CA5B PIP5K1B WNT9A CCNH GEM IL18RAP GGH SARDH B3GNT7 C13orf46 SBF2 IKZF3 ZMAT1 TCF7 NECTIN1 H3C7 FOS PAG1 HECA SLC4A10 SLC35G2 PER1 P2RY1 NFKBIA WDR76 PLAUR KDM1A H1-5 TSHZ2 FAM102B HMMR GPR132 CCRL2 PARP8 A2M ST8SIA1 NUF2 IL5RA RBPMS UBE2T USP53 EEF1A1 PLAC8 LGR6 TMEM123 NEK2 SNAP47 PTGIS SH2B3 P2RY8 S100PBP PLEKHA7 CLNK CRIM1 MGAT5 YBX3 TP53INP1 DTL CFH FEZ1 MYB FRMD4B TSPAN5 STIL ITGA2 GOLGA6L10 MYBL2 AHI1 CAND2 GZMB RBPJ PELI1 HSPA1B KCNK5 GOLGA6L9 TICRR TPRG1 UBE2C AURKA Leem G, et al.
    [Show full text]
  • Cellular and Molecular Signatures in the Disease Tissue of Early
    Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of
    [Show full text]
  • Anti-SIRPG Monoclonal Antibody, Clone OX119 (CABT-53873MH) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
    Anti-SIRPG monoclonal antibody, clone OX119 (CABT-53873MH) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Product Overview Mouse anti Human CD172g antibody, clone OX119 recognizes human SIRP gamma, a 55kD signal regulatory protein which is a member of the immunoglobulin gene superfamily. SIRP gamma, also known as CD172g, is expressed on most T lymphocytes and a subset of B-cells but is absent on myeloid cells. CD172g has a truncated cytoplasmic tail, which is similar to SIRP beta, but unlike SIRP beta CD172g does not require DAP12 for expression at the cell surface. CD172g, like SIRP alpha, binds to CD47 inducing apoptosis. It is also involved in the negative regulation of receptor tyrosine kinase-coupled signalling. Flow Cytometry Use 10ul of the suggested working dilution to label 1x106 cells in 100ul. Specificity SIRPG Immunogen Purified recombinant SIRPgamma.CD4. Isotype IgG1 Source/Host Mouse Species Reactivity Human Clone OX119 Conjugate Unconjugated Applications FC; IP Format Purified IgG - liquid Size 200 μg Preservative 0.09% Sodium Azide Storage in frost-free freezers is not recommended. This product should be stored undiluted. Avoid repeated freezing and thawing as this may denature the antibody. Should this product contain a precipitate we recommend microcentrifugation before use. Warnings For research purposes only 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved
    [Show full text]
  • Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
    Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase
    [Show full text]
  • A Novel Foxp3-Related Immune Prognostic Signature for Glioblastoma Multiforme Based on Immunogenomic Profiling
    www.aging-us.com AGING 2021, Vol. 13, No. 3 Research Paper A novel foxp3-related immune prognostic signature for glioblastoma multiforme based on immunogenomic profiling Xiao-Yu Guo1,*, Guan-Hua Zhang1,2,*, Zhen-Ning Wang1, Hao Duan1, Tian Xie1, Lun Liang1, Rui Cui1, Hong-Rong Hu1, Yi Wu3, Jia-jun Dong3, Zhen-Qiang He1, Yong-Gao Mou1 1Department of Neurosurgery AND Neuro-Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510000, China 2Department of Cerebrovascular Surgery, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510000, China 3Department of Neurosurgery, Jiangmen Central Hospital, Jiangmen 529030, China *Equal contribution Correspondence to: Yong-Gao Mou, Zhen-Qiang He; email: [email protected], [email protected] Keywords: glioblastoma multiforme, Foxp3, regulatory T cells, immune prognostic signature, nomogram Received: June 8, 2020 Accepted: October 31, 2020 Published: January 10, 2021 Copyright: © 2021 Guo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Foxp3+ regulatory T cells (Treg) play an important part in the glioma immunosuppressive microenvironment. This study analyzed the effect of Foxsp3 on the immune microenvironment and constructed a Foxp3-related immune prognostic signature (IPS)for predicting prognosis in glioblastoma multiforme (GBM). Immunohistochemistry (IHC) staining for Foxp3 was performed in 72 high-grade glioma specimens. RNA-seq data from 152 GBM samples were obtained from The Cancer Genome Atlas database (TCGA) and divided into two groups, Foxp3 High (Foxp3_H) and Foxp3 Low (Foxp3_L), based on Foxp3 expression.
    [Show full text]
  • Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association Between BMI and Adult-Onset Non- Atopic
    Supplementary Material DNA Methylation in Inflammatory Pathways Modifies the Association between BMI and Adult-Onset Non- Atopic Asthma Ayoung Jeong 1,2, Medea Imboden 1,2, Akram Ghantous 3, Alexei Novoloaca 3, Anne-Elie Carsin 4,5,6, Manolis Kogevinas 4,5,6, Christian Schindler 1,2, Gianfranco Lovison 7, Zdenko Herceg 3, Cyrille Cuenin 3, Roel Vermeulen 8, Deborah Jarvis 9, André F. S. Amaral 9, Florian Kronenberg 10, Paolo Vineis 11,12 and Nicole Probst-Hensch 1,2,* 1 Swiss Tropical and Public Health Institute, 4051 Basel, Switzerland; [email protected] (A.J.); [email protected] (M.I.); [email protected] (C.S.) 2 Department of Public Health, University of Basel, 4001 Basel, Switzerland 3 International Agency for Research on Cancer, 69372 Lyon, France; [email protected] (A.G.); [email protected] (A.N.); [email protected] (Z.H.); [email protected] (C.C.) 4 ISGlobal, Barcelona Institute for Global Health, 08003 Barcelona, Spain; [email protected] (A.-E.C.); [email protected] (M.K.) 5 Universitat Pompeu Fabra (UPF), 08002 Barcelona, Spain 6 CIBER Epidemiología y Salud Pública (CIBERESP), 08005 Barcelona, Spain 7 Department of Economics, Business and Statistics, University of Palermo, 90128 Palermo, Italy; [email protected] 8 Environmental Epidemiology Division, Utrecht University, Institute for Risk Assessment Sciences, 3584CM Utrecht, Netherlands; [email protected] 9 Population Health and Occupational Disease, National Heart and Lung Institute, Imperial College, SW3 6LR London, UK; [email protected] (D.J.); [email protected] (A.F.S.A.) 10 Division of Genetic Epidemiology, Medical University of Innsbruck, 6020 Innsbruck, Austria; [email protected] 11 MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, W2 1PG London, UK; [email protected] 12 Italian Institute for Genomic Medicine (IIGM), 10126 Turin, Italy * Correspondence: [email protected]; Tel.: +41-61-284-8378 Int.
    [Show full text]
  • Cancer-Specific Immune Prognostic Signature in Solid Tumors and Its Relation to Immune Checkpoint Therapies
    Cancers 2020, 12 S1 of S8 Supplementary Materials: Cancer-Specific Immune Prognostic Signature in Solid Tumors and Its Relation to Immune Checkpoint Therapies Shaoli Das, Kevin Camphausen and Uma Shankavaram Supplementary Figures Figure S1. ssGSEA of scRNA-seq data of tumor samples from four solid tumor histologies (breast, colon, glioblastoma, and head and neck tumors) identifies three or two dominant immune-function- associated cell clusters. One of these clusters is enriched for monocytes, macrophages, dendritic cells (MoMaDC), another cluster is enriched for NK-, T-cells, and another is enriched for B-cell functions. For head and neck tumors and glioblastomas, B-cell enrichments does not form a distinct cluster but forms a unified cluster along with NK- and T-cells. (a) Analysis of a breast cancer scRNA-seq data set identifies nine cell clusters from unsupervised t-SNE clustering. (b) These clusters were assigned to three distinct sets of immune functions using ssGSEA, as seen from the heat map (one related to monocytes, macrophages, TLR and dendritic cells; one related to B-cell functions; and the other related to NK- and T-cell functions). (c) The stacked bar plot shows that cell clusters 1, 3, and 4 are enriched for functions related to monocytes, macrophages, and dendritic cells; the cell cluster 6 is enriched for B cell functions; and cell cluster 7 is enriched for NK- and T- related functions. (d) Analysis of a GBM scRNA-seq data set identifies 10 cell clusters from unsupervised t-SNE clustering. (e) These clusters were assigned to two distinct sets of immune functions using ssGSEA, as seen from the heat map (one related to monocytes, macrophages, TLR, dendritic cells and the other related to NK-, T- and B-cell functions).
    [Show full text]
  • Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
    BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the filtration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green fluorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in
    [Show full text]
  • Human RELT/TNFRSF19L Antibody Antigen Affinity-Purified Polyclonal Goat Igg Catalog Number: AF1385
    Human RELT/TNFRSF19L Antibody Antigen Affinity-purified Polyclonal Goat IgG Catalog Number: AF1385 DESCRIPTION Species Reactivity Human Specificity Detects human RELT/TNFRSF19L in direct ELISAs and Western blots. In direct ELISAs, less than 1% cross­reactivity with recombinant human (rh) 4­1BB, rhBAFF R, rhCD27, rhTAJ, rhCD30, rhDR3, rhDR6, rhTNF RI, rhTNF RII, rhEDAR, rhFas, rhGITR, rhHVEM, rhNGF R, rhOPG, and recombinant mouse OX40 is observed. Source Polyclonal Goat IgG Purification Antigen Affinity­purified Immunogen Mouse myeloma cell line NS0­derived recombinant human RELT/TNFRSF19L Ser26­Ala160 (Arg127Gly, Arg129Gly) Accession # Q969Z4 Formulation Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. See Certificate of Analysis for details. *Small pack size (­SP) is supplied either lyophilized or as a 0.2 μm filtered solution in PBS. APPLICATIONS Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website. Recommended Sample Concentration Western Blot 1 µg/mL See Below DATA Western Blot Detection of Human RELT/TNFRSF19L by Western Blot. Western blot shows lysates of human bone marrow tissue and human lymph node tissue. PVDF membrane was probed with 1 µg/mL of Goat Anti­Human RELT/TNFRSF19L Antigen Affinity­purified Polyclonal Antibody (Catalog # AF1385) followed by HRP­conjugated Anti­Goat IgG Secondary Antibody (Catalog # HAF017). A specific band was detected for RELT/TNFRSF19L at approximately 50 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1. PREPARATION AND STORAGE Reconstitution Reconstitute at 0.2 mg/mL in sterile PBS.
    [Show full text]