DOCSLIB.ORG

2823.Full.Pdf

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
2823.Full.Pdf Report on the 2018 Cancer, Autoimmunity, and Immunology Conference Colleen S. Curran, Connie L. Sommers, Howard A. Young, Katarzyna Bourcier, Marie Mancini and Elad Sharon This information is current as of September 28, 2021. J Immunol 2019; 202:2823-2828; Prepublished online 15 April 2019; doi: 10.4049/jimmunol.1900264 http://www.jimmunol.org/content/202/10/2823 Downloaded from References This article cites 15 articles, 6 of which you can access for free at: http://www.jimmunol.org/content/202/10/2823.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 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Report on the 2018 Cancer, Autoimmunity, and Immunology Conference † ‡ x Colleen S. Curran,*{ Connie L. Sommers,‖ Howard A. Young, Katarzyna Bourcier, Marie Mancini, and Elad Sharon With the increased use of cancer immunotherapy, a immune-related adverse events (irAEs) that accompany cancer number of immune-related adverse events (irAEs) are immunotherapy. After an introduction to the recent history being identified. These irAEs can be compared with of cancer immunotherapy and the definition and recognition known autoimmune disorders in similar tissues, with of irAEs by Anthony Fauci (National Institute of Allergy important similarities and differences. Understanding and Infectious Diseases [NIAID]), Dr. Topalian focused on the etiology of irAEs may bring to light concepts appli- irAEs that result from immune checkpoint blockade therapy. cable to immune responses in cancer, autoimmunity, She described how T cells are activated by signal 1 (through Downloaded from and infectious disease. This immunobiology is espe- the T cell Ag receptor) and signal 2 (through coreceptors). cially relevant to cancer patients with preexisting allo- Checkpoint molecules expressed on the surface of T cells (such geneic transplants or autoimmune disease who are as PD-1 and CTLA-4) normally restrain the T cell activation undergoing cancer immunotherapy. To address these response from becoming too long or out of control. Drugs such as nivolumab (anti–PD-1) and ipilimumab (anti-CTLA4) facets of cancer immunotherapy, academic leaders from interfere with that control in a process commonly referred to as http://www.jimmunol.org/ these various disciplines discussed current irAE basic “releasing the brakes” on T cells. Dr. Topalian discussed how and clinical research, irAE diagnosis and management, different immune checkpoint inhibitors have different mecha- and the need for biomarkers and algorithms to identify nisms of action and different frequencies of associated irAEs. individuals at risk for irAEs at a conference jointly spon- Studies of the etiology of irAEs could help elucidate mech- sored by the National Cancer Institute, National Insti- anisms of antitumor activity, as irAE frequency tends to tute of Allergy and Infectious Diseases, and National associate with higher antitumor response. Institute of Arthritis and Musculoskeletal and Skin Dis- As noted by Dr. Bluestone, these irAEs may also provide eases in Bethesda, MD, on March 22–23, 2018. Mech- deeper understanding of the basic immunological mechanisms by guest on September 28, 2021 anisms and models to characterize irAEs, standardize underlying autoimmune conditions. The cross-talk among these protocols, store biospecimens, and capture and analyze specialties has enormous potential for reverse translation in the irAE data were also reviewed during the inaugural fields of cancer, autoimmunity, and immunology. Continued Cancer, Autoimmunity, and Immunology Conference. research into the basic biological responses to immune check- This summary highlights cancer immunotherapy– point inhibitors and other forms of immunotherapy is needed induced irAEs, the challenges ahead, and the oppor- to further define the mechanisms of action, diagnosis, treatment, tunities for greater understanding of autoimmune and management of distinct irAEs that are now being observed conditions. The Journal of Immunology, 2019, 202: in clinical trials and standard oncology practice. 2823–2828. Murine models of irAEs eynote speakers Suzanne Topalian (Johns Hopkins Although human irAEs are not completely reproducible in University) and Jeffrey Bluestone (Parker Institute mice, a number of models have been developed that add to K for Cancer Immunotherapy [PICI] and University our knowledge of immunotherapy-induced irAEs. Keynote of California–San Francisco) introduced each of the morn- speaker Jeffrey Bluestone emphasized that in the future, we ing sessions of the 2-day conference that detailed the biology, should attempt to predict which drug combinations will diagnosis, treatment, management, and the implications of provide robust antitumor effects without irAEs, provided *Department of Critical Care Medicine, Clinical Center, National Institutes of Health, Received for publication March 4, 2019. Accepted for publication March 22, 2019. Bethesda, MD 20892; †ImmunoOncology Branch, Developmental Therapeutics Pro- Address correspondence and reprint requests to Dr. Elad Sharon, National Cancer gram, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National ‡ Institute, National Institutes of Health, 9609 Medical Center Drive, Room 5W512, Institutes of Health, Rockville, MD 20850; Cancer and Inflammation Program, Center Bethesda, MD 20892. E-mail address: [email protected] for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, x MD 21702; Division of Allergy, Immunology, and Transplantation, National Institute Abbreviations used in this article: allo-HSCT, allogeneic hematopoietic stem cell trans- of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852; plantation; FDA, Food and Drug Administration; GVHD, graft-versus-host disease; { Systemic Autoimmune Disease Biology Program, Division of Extramural Research, irAE, immune-related adverse event; NCI, National Cancer Institute; NIAID, National National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Insti- Institute of Allergy and Infectious Diseases; PICI, Parker Institute for Cancer ‖ tutes of Health, Bethesda, MD 20892; and Cancer Therapy Evaluation Program, Immunotherapy. Division of Cancer Treatment and Diagnosis, National Cancer Institute, National In- stitutes of Health, Bethesda, MD 20892 ORCIDs: 0000-0002-3118-5111 (H.A.Y.); 0000-0002-0044-9719 (E.S.). www.jimmunol.org/cgi/doi/10.4049/jimmunol.1900264 2824 CANCER, AUTOIMMUNITY, AND IMMUNOLOGY CONFERENCE that well-characterized syngeneic mouse models can be de- of immune-related toxicity in specific organs. In identifying veloped. Further, it will be important for clinicians to choose genetic signatures of immune cells, tumor cells, and stromal the best combination for patients who may be predisposed to cells in the tumor microenvironment, researchers may ef- different subclinical autoimmune conditions and may develop fectively predict responders, nonresponders, and/or patient particular irAEs. Different mouse models with distinct auto- subsets susceptible to irAEs from patient biopsies. One immune tendencies can shed light on these issues. Wild-type approach, as described by both Emanual Maverakis (University mice can also be useful for immunotherapy research, as of California–Davis) and Orit Rozenblatt-Rosen (Broad evidenced by the work of Patrizio Caturegli (Johns Hopkins Institute), involves cross-comparing RNA sequencing data University). His studies in wild-type mice revealed the ex- obtained from tumor samples from patients who have ei- pression of CTLA-4 in the pituitary, which provides the likely ther responded or failed to respond to immune checkpoint mechanistic basis for the hypophysitis that can occasionally blockade with bulk gene expression data from samples develop in patients undergoing anti–CTLA-4 immunotherapy uploaded in The Cancer Genome Atlas. Researchers can (1) (Fig. 1A). Mice with genetic deletion of CTLA-4, PD-1, also compare the gene signatures retrieved from autoimmune and/or PD-L1 have revealed defects in T cell tolerance and and cancer patients. David Hafler (Yale University) provided display various degrees of autoimmunity. As explained by an example of melanoma patients with a BRAFV600K mutation Javid Moslehi (Vanderbilt University), myocarditis occurs that may develop myelin-autoreactive T cells subsequent to 2 2 2 2 2 2 in CTLA-4 / micecrossedwithPD-L1 / or PD-1 / anti–CTLA-4 therapy, similar to T cells found in multiple mice (2), suggesting that combination therapies may increase sclerosis patients (4). Ignacio Sanz (Emory University) indi- Downloaded from the risk for the development of myocardial inflammation cated that next-generation sequencing of TCRs and BCRs, as (Fig. 1B). IFN-g–induced PD-L1 expression on mouse heart well
Load more

Recommended publications
  • Regulatory T Cells (Tregs): Frequently Asked Questions
    BD Biosciences Technical Resources Page 1 December 2010 Regulatory T Cells (Tregs): Frequently Asked Questions What are the differences between natural Tregs and inducible Tregs? Natural Tregs (nTregs) originate from the thymus as CD4+CD25+ cells together with expression of the transcription factor FoxP3 and aren’t really influenced by the cytokine milieu. Natural Tregs represent approximately 5–10% of the total CD4+ T-cell population. They are thought to be positively selected during thymic selection, with a relatively high avidity for self-antigens. The signal to develop into Tregs is thought to come from interactions between the T-cell receptor and the complexes of MHC II with self-peptide expressed on the thymic stroma and is observed at the single-positive stage of T-lymphocyte development. On the other hand, inducible Tregs (iTregs) originate as CD4 single-positive cells from the thymus, and following adequate antigenic stimulation in the presence of cognate antigen and specialized immunoregulatory cytokines such as TGF-β, IL-10, and IL-4, differentiate into CD25+ and FoxP3+ expressing Tregs—hence called “adaptive” or “inducible” Tregs. Adaptive or inducible T cells are further categorized into Tr1, Th2, or Tr3 depending on the cytokines that modulate them.1,2 Are there any differences between mouse and human CD4+ Tregs? Yes there are. In mice, CD4+ Tregs are a homogenous population, in which all CD4+ and CD25+ cells are regulatory T cells. In humans, the Tregs are a heterogeneous population, in which not all CD25+ cells are Tregs. This was first observed by a detailed analysis of human CD4+CD25+ populations by groups at Harvard and the Royal Free and University College Medical School in London.3,4 Studies revealed that only those CD4+ cells that expressed very high levels of CD25, representing approximately 2–3% of total CD4 T cells, demonstrate the in vitro suppressive activity similar to that described in murine cells.
    [Show full text]
  • Donor-Alloantigen-Reactive Regulatory T Cell Therapy in Liver
    Confidential Page 1 of 80 Donor-Alloantigen-Reactive Regulatory T Cell Therapy in Liver Transplantation Version 7.0/ August 1, 2018 IND# 15479 Study Sponsor(s): The National Institute of Allergy and Infectious Diseases (NIAID) Grant #: R34AI095135 and U01AI110658-01 Study Drug Manufacturer/Provider: Sanofi US PRINCIPAL INVESTIGATOR CO- PRINCIPAL INVESTIGATOR CO- PRINCIPAL INVESTIGATOR SANDY FENG, MD, PHD JEFFREY BLUESTONE, PHD SANG-MO KANG, MD, FACS Professor of Surgery Executive Vice Chancellor and Provost Associate Professor Director, Abdominal Transplant A.W. Clausen Distinguished Professor University of California, San Surgery Fellowship in Medicine Francisco University of California, San University of California, San Francisco 513 Parnassus Ave. Francisco 513 Parnassus Ave. Box 0780, HSE-520 505 Parnassus Ave. Box 0400, HSW-1128 San Francisco, CA 94143-0780 Box 0780, M-896 San Francisco, CA 94143-0780 Phone: (415) 353-1888 San Francisco, CA 94143-0780 Phone: (415) 476-4451 E-mail: Sang- Phone: (415) 353-8725 Fax: (415) 476-9634 [email protected] Fax: (415) 353-8709 E-mail: [email protected] E-mail: [email protected] CO- PRINCIPAL INVESTIGATOR BIOSTATISTICIAN MEDICAL OFFICER QIZHI TANG, PHD DAVID IKLÉ, PHD NANCY BRIDGES, MD Associate Professor Senior Statistical Scientist Chief, Transplantation Branch Director, UCSF Transplantation Rho, Inc. Division of Allergy, Immunology, Research Lab 6330 Quadrangle Drive and Transplantation University of California, San Chapel Hill, NC 27517 NIAID Francisco Phone: (910) 558-6678
    [Show full text]
  • At FOCIS 2016
    SAVE THE DATE Immunology by the Bay KEYNOTE SPEAKERS: Frank Nestle, MD Lewis Lanier, PhD King's College London University of California, San Francisco IMMUNOTHERAPY From Pathogens to Autoimmunity to Cancer FOCIS 2016 Supporters FOCIS gratefully acknowledges the support that allows FOCIS to fulfill its mission to foster interdisciplinary approaches to both understand and treat immune-based diseases, and ultimately to improve human health through immunology. Platinum Level Sponsors Gold Level Sponsors Silver Level Sponsors Immune Tolerance Network Bronze Level Sponsors Copper Level Sponsors Thank you to the FOCIS 2016 Travel Award Supporters: Dear Colleagues, Welcome to the 16th annual meeting of the Federation of Clinical Immunology Societies, FOCIS 2016. I am partic- ularly excited about this year’s meeting. The scientific program reflects the core tenets of FOCIS by bridging the gap between basic and clinical immunology and discussing novel translational therapies. We value the participation of each of you who have touched FOCIS in one way or another over the past 16 years, and we hope that you will join us as we move into the future. FOCIS introduced individual membership in 2012, and I invite you to join FOCIS and collaborate with us to promote education, research and patient care around the theme of translational immunology. Memberships run on a calendar year basis and are available at reasonable prices. At FOCIS 2016, membership also gains you exclusive access to a Members Only Lounge complete with a complimentary espresso bar as well as a Pushing the hip Members Only Reception in the Lighthouse on Thursday, June 23. boundaries of Please join me in extending my most heartfelt thanks to the members of the FOCIS 2016 Scientific Program Committee for their time, energy and expertise.
    [Show full text]
  • Safety and Efficacy of Imatinib for Preserving Beta-Cell Function in New- Onset Type 1 Diabetes Mellitus
    Safety and Efficacy of Imatinib for Preserving Beta-cell Function in New- onset Type 1 Diabetes Mellitus Version:8.0 August 23, 2016 IND # 117,644 Sponsored by the Juvenile Diabetes Research Foundation International (JDRF). CONFIDENTIAL Page 1 SAFETY AND EFFICACY OF IMATINIB FOR PRESERVING BETA-CELL FUNCTION IN NEW-ONSET TYPE 1 DIABETES MELLITUS Version 7.0 ( January 29, 2016) IND # 117,644 Protocol Co-Chair Protocol Co-Chair Jeffrey A. Bluestone, Ph.D. Stephen E. Gitelman, MD Professor of Medicine, Pathology, Professor of Clinical Pediatrics Microbiology & Immunology Department of Pediatrics University of California, San Francisco University of California, San Francisco Campus Box 0540 Room S-679, Campus Box 0434 513 Parnassus Avenue 513 Parnassus Avenue San Francisco, CA 94143 San Francisco, CA 94143 Tel: 415-514-1683 Fax: 415-564-5813 Tel: 415-476-3748 Fax: 415-476-8214 Email: [email protected] Email: [email protected] This clinical study is supported by JDRF and conducted by the University of California, San Francisco. This document is confidential. It is provided for review only to investigators, potential investigators, consultants, study staff, and applicable independent ethics committees or institutional review boards. It is understood that the contents of this document will not be disclosed to others without written authorization from the study sponsor unless it is necessary to obtain informed consent from potential study participants. Imatinib in New-onset T1DM Protocol Final Version 8.0 August 23, 2016 CONFIDENTIAL Page 2 Protocol Approval Trial ID: Protocol Version: 8.0 Dated: August 23, 2016 IND # 117,644 Protocol Chairs: Jeffrey Bluestone, PhD and Stephen Gitelman, MD Title: Safety and Efficacy of Imatinib for Preserving ß-cell Function in New-onset Type 1 Diabetes Mellitus I confirm that I have read the above protocol in the latest version.
    [Show full text]
  • Cancer-Immunotherapy-Article.Pdf
    Corrected 26 March 2018. See full text. CANCER IMMUNOTHERAPY REVIEW toxicities resulting from tissue-specific inflam- mation (4, 5). The most common of these toxic- ities included enterocolitis, inflammatory hepatitis, and dermatitis. Algorithmic use of corticoste- Cancer immunotherapy using roidsorotherformsofimmunesuppressionreadily controlled these symptoms without any appar- checkpoint blockade ent loss of antitumor activity (6). However, less frequent adverse events also included inflamma- Antoni Ribas1* and Jedd D. Wolchok2,3* tion of the thyroid, pituitary, and adrenal glands, with the need for lifelong hormone replacement. The release of negative regulators of immune activation (immune checkpoints) that Clinical activity of CTLA-4 blockade was most limit antitumor responses has resulted in unprecedented rates of long-lasting apparent in patients with advanced metastatic tumor responses in patients with a variety of cancers. This can be achieved by antibodies melanoma, with a 15% rate of objective radio- blocking the cytotoxic T lymphocyte–associated protein 4 (CTLA-4) or the programmed graphic response that has been durable in some cell death 1 (PD-1) pathway, either alone or in combination. The main premise for patients for >10 years since stopping therapy inducing an immune response is the preexistence of antitumor T cells that were limited (7, 8). The patterns of clinical response shown by by specific immune checkpoints. Most patients who have tumor responses maintain radiographic imaging after ipilimumab were some- long-lasting disease control, yet one-third of patients relapse. Mechanisms of acquired times distinct from those associated with therapies resistance are currently poorly understood, but evidence points to alterations that have more direct antiproliferative mecha- that converge on the antigen presentation and interferon-g signaling pathways.
    [Show full text]
  • AST 2015 Achievement Award and Grant Press Release
    FOR IMMEDIATE RELEASE Media Contact: Cate Girone 856-793-0796 [email protected] THE AMERICAN SOCIETY OF TRANSPLANTATION ANNOUNCES 2015 ACHIEVEMENT AWARD AND GRANT RECIPIENTS The American Society of Transplantation (AST) announced the recipients of the 2015 Achievement Awards and the Faculty and Fellowship Grants at the recent American Transplant Congress (ATC) in Philadelphia. The recipients were selected for their achievements and contributions to the AST and to the field of transplantation. “This year’s award recipients are an inspiring group of transplantation professionals. They have been selected by their peers for the transformative role they have each played in shaping our field,” said AST President Dr. James Allan. “We applaud them for their dedication and success.” AST Achievement Awards AST Senior Achievement in Clinical Transplantation Award – Gabriel Danovitch, MD, David Geffen School of Medicine at UCLA Dr. Danovitch has contributed more than three decades of service to the field of transplantation and nephrology. He is a world-renowned transplant physician whose work spans the entire spectrum of clinical activities in transplantation, from innovative research to superb patient care. AST Mentoring Award – Jeffrey Bluestone, PhD, Diabetes Center at University of California, San Francisco Dr. Bluestone has mentored over eighty students, post-doctoral fellows, and research associates. Thirty of his trainees have gone on to become university-based academicians throughout the United States and abroad. Several of his trainees have become transplantation professionals with leadership positions in the AST, including Dr. Kenneth Newell, immediate past-president. AST Transplant Advocacy Award – William Applegate, Bryan Cave LLP Currently the Senior Vice President of Bryan Cave LLP and Director of Government Relations, Mr.
    [Show full text]
  • Regulatory T Cells: Essential Regulators of the Immune System
    Regulatory T Cells: Essential Regulators of the Immune System Tools for the identification, isolation, and multicolor analysis of human regulatory T cells CD4+ CD8+ CD4+ CD45RO+ An tige + n Sti CD25 mulation FoxP3- CD4+ CD4+ Memory T Cell CD25high Naïve T Cell FoxP3+ CD4+ CD25- FoxP3- Natural Treg β + IL-10 CD4 and/or TGF Induced Treg CD25low Th17 FoxP3+ low + CD25 CD4 CD25low CD4+ CD25high Th2 CD4+ Th1 A proven commitment to regulatory T cell research As evidence of the immunosuppressive potential of T cells has developed in recent years, interest in Regulatory T cells (Tregs) and enthusiasm for their potential therapeutic application has intensified. Thus Treg research is very active, and new publications emerge almost daily. Today the most commonly used markers for Treg identification, isolation, and characterization are CD4, CD25, CD127, and FoxP3. However, new targets with functional significance such as CD39, CD45RA, CTLA-4, and others are rapidly emerging. For over 20 years, BD Biosciences has actively supported groundbreaking research in the field. With a rich portfolio of high quality immunology products, BD Pharmingen™ brand reagents support both established markers as well as emerging trends in this dynamic envi- ronment. With new discoveries about the role of proteins in Tregs, many existing markers gain new utility. This proven commitment to help advance discovery in Treg research is the foundation of BD Biosciences ongoing efforts to provide a full range of tools to simplify the identification, isolation and characterization of Treg cells and their interacting partners. BD Biosciences reagents are backed by a world-class service and support organization to help customers take full advantage of our products to advance their research.
    [Show full text]
  • National Cancer Advisory Board Blue Ribbon Panel Roster
    June 2016 NATIONAL INSTITUTES OF HEALTH NATIONAL CANCER INSTITUTE NATIONAL CANCER ADVISORY BOARD BLUE RIBBON PANEL CO-CHAIRS Tyler E. Jacks, Ph.D. Director Koch Institute for Integrative Cancer Research David H. Koch Professor of Biology Massachusetts Institute of Technology Cambridge, MA Elizabeth M. Jaffee, M.D. Deputy Director The Sidney Kimmel Comprehensive Cancer Center The Dana and Albert “Cubby” Broccoli Professor of Oncology Co-Director, Skip Viragh Center for Pancreas Cancer The Johns Hopkins University Baltimore, MD Dinah S. Singer, Ph.D. Acting Deputy Director Director, Division of Cancer Biology National Cancer Institute National Institutes of Health Bethesda, MD MEMBERS Peter C. Adamson, M.D. Mary C. Beckerle, Ph.D. Chair, Children's Oncology Group Ralph E. and Willia T. Main Presidential Professor Alan R. Cohen Endowed Chair in Pediatrics Chief Executive Officer and Director The Children's Hospital of Philadelphia Huntsman Cancer Institute Philadelphia, PA Associate Vice President of Cancer Affairs Distinguished Professor of Biology James P. Allison, Ph.D. University of Utah Chairman of Immunology Salt Lake City, UT Department of Immunology The University of Texas Mitchel S. Berger, M.D. MD Anderson Cancer Center Professor and Chair Houston, TX Department of Neurological Surgery University of California, San Francisco San Francisco, CA David F. Arons, J.D. Chief Executive Officer Jeffrey Bluestone, Ph.D. National Brain Tumor Society A.W. and Mary Margaret Clausen Distinguished Newton, MA Professor Director, Hormone Research Institute Emeritus Executive Vice Chancellor and Provost University of California, San Francisco San Francisco, CA June 2016 Chi V. Dang, M.D., Ph.D. Lifang Hou, MD., MS, Ph.D Professor of Medicine Associate Professor Division of Hematology-Oncology Chief, Division of Cancer Epidemiology and Department of Medicine Prevention Director, Abramson Cancer Center Department of Preventive Medicine & Co-Director, International Relations Director, Abramson Cancer Research Institute Robert H.
    [Show full text]
  • Powerful Connections CHAIRMAN’S MESSAGE
    powerful connections CHAIRMAN’S MESSAGE I am delighted to present to you the 2017 Department of Medicine Annual Report entitled table of contents “Powerful Connections”. Connections that bridge our programs and people are so important to enhancing our missions of discovery, innovative patient care and mentorship. Connections are fun- damental to science and medicine. Across departments scientists connect scientific findings from bench to bedside and back with the goal of improving patient outcomes and developing better ther- apies, and our medical educators channel their knowledge to our trainees to enhance the learning environment and prepare them for their academic careers. Chair’s message 1 Cardiology 14 Some examples from the last year include: • The appointment of four new administrative Clinically, the Department of Medicine continued Organization 2 Computational Biomedicine • The discovery that the onset of Celiac disease leaders, Matthew Sorrentino, MD as Vice Chair to impact patient care with new initiatives and and Biomedical Data Science 16 could be triggered by prior Reovirus infection for Clinical Operations, Steven White, MD as connections in the community, city, and region. Medicine by the Numbers 3 (Jabri) Associate Vice Chair for Appointments and This included the expansion of the Department’s Dermatology 18 Promotions, Anne Sperling, PhD as Associate clinical imprint at the University of Chicago Special Awards 4 • The preclinical development of novel approach- Vice Chair for Research and Julie White as Medicine’s new offsite practices in Orland Park Emergency Medicine 20 es to prostate cancer immunotherapy using a Executive Administrator and Chicago’s South Loop, at Ingalls Hospital Faculty Highlights 6 tyrosine kinase inhibitor to infiltrate and clear the as well as at satellite clinics in Indiana.
    [Show full text]
  • TCR-Transgenic T Cells + Than B7.2 in the Activation of Naive CD8 B7.1 Is a Quantitatively Stronger Costimulus
    B7.1 Is a Quantitatively Stronger Costimulus Than B7.2 in the Activation of Naive CD8 + TCR-Transgenic T Cells This information is current as Patrick E. Fields, Rosalynde J. Finch, Gary S. Gray, Richard of September 28, 2021. Zollner, Jenifer L. Thomas, Knut Sturmhoefel, Kwan Lee, Stanley Wolf, Thomas F. Gajewski and Frank W. Fitch J Immunol 1998; 161:5268-5275; ; http://www.jimmunol.org/content/161/10/5268 Downloaded from References This article cites 33 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/161/10/5268.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 © 1998 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. B7.1 Is a Quantitatively Stronger Costimulus Than B7.2 in the Activation of Naive CD81 TCR-Transgenic T Cells1 Patrick E. Fields,* Rosalynde J. Finch,‡ Gary S.
    [Show full text]
  • UCSF Department of Medicine Department UCSF and Apatient
    SCROLL TO LAST PAGE FOR ARTICLE UCSF Department of Medicine FRONTIERS OF MEDICINE ISSUE 24 / SPRING 2017 CONTENTS Unleashing the Army Within 1 From the Chair 2 Alumni Profile: 3 Dr. Margaret Callahan The Parker Institute 8 for Cancer Immunotherapy Faculty Profile: 9 Dr. Lawrence Fong New Department 10 Chair Profile: Dr. Robert M. Wachter Appointments 11 Donor Profile: 12 Peter Michael Foundation Oncologist Lawrence Fong, MD (center), who co-leads the UCSF Cancer Immunotherapy Clinic, consults with Gabriel N. Mannis, MD (left), Cancer Immunotherapy and a patient. Unleashing the Army Within What if the human body possessed a powerful weapon against cancer, honed by millions of years of evolution? That’s the idea behind immunotherapy, one of the most promising new approaches to fighting cancer. Instead of directly trying to poison cancer cells with chemotherapy, immunotherapy boosts the body’s own immune system to attack cancer cells – the same way it kills viruses and bacteria. Long before cancer immunotherapy made headlines by helping former President Jimmy Carter achieve remission from metastatic melanoma – a disease which often kills people within months – UCSF Department of Medicine faculty members had been working to translate an intriguing idea into remarkably potent therapies. “Cancer immunotherapy has been something that people have thought about for decades, but the real excitement now is we’ve made the transition from pre-clinical studies and animal models to actually treating patients,” said oncologist Lawrence Fong, MD, Efim Guzik Distinguished Professor in Cancer Biology. He co-leads the UCSF Cancer Immunotherapeutics Program, established in April 2016, which includes both a clinic that offers the latest immunotherapy drugs to patients through continued on page 4 UCSF DEPARTMENT OF MEDICINE UCSF DEPARTMENT Editorial Advisory Board: From the Chair Robert M.
    [Show full text]
  • Scientific Program
    SCIENTIFIC PROGRAM FOCIS 2017 1 SPONSORS PLATINUM LEVEL GOLD LEVEL SILVER LEVEL BRONZE LEVEL Thank you to the FOCIS 2017 Travel Award Supporters: 2 FOCIS 2017 Dear Colleagues, Welcome to the 17th annual meeting of the Federation of Clinical Immunology Societies, FOCIS 2017. I am particularly excited about this year’s meeting. The scientific program reflects the core tenets of FOCIS by bridging the gap between basic and clinical immunology and discussing novel translational therapies. We value the participation of each of you who have touched FOCIS in one way or another over the past 17 years, and we hope that you will join us as we move into the future. FOCIS introduced individual membership in 2012, and I invite you to join FOCIS and collaborate with us to promote education, research and patient care around the theme of translational immunology. Memberships run on a calendar year basis and are available at the conference. At FOCIS 2017, membership also gains you exclusive access to a Members-only Lounge complete with a complimentary espresso bar as well as a festive Members-only Reception at Kitty O’Sheas on Thursday, June 16. Please join me in extending my most heartfelt thanks to the members of the FOCIS 2017 Scientific Program Committee for their time, energy and expertise. I hope you enjoy the fruits of their labor – FOCIS 2017. Welcome to Chicago! Sincerely, Jeffrey Bluestone, PhD, FOCIS President University of California, San Francisco FOCIS 2017 MOBILE APP Use your mobile phone/tablet to view the program, make SUPPORTERS a personal schedule, view the exhibits and much more! ACKNOWLEDGEMENTS: FOCIS gratefully acknowledges the support that allows FOCIS to fulfill its mission to foster interdisciplinary approaches to both understand and treat immune- based diseases, and ultimately to improve human health through immunology.
    [Show full text]