DOCSLIB.ORG

And Enhance Igg2a Production in Vivo HLA-DM-Sufficient Antigen

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
And Enhance Igg2a Production in Vivo HLA-DM-Sufficient Antigen Chemical Chaperones Enhance Superantigen and Conventional Antigen Presentation by HLA-DM-Deficient as well as HLA-DM-Sufficient Antigen-Presenting Cells This information is current as and Enhance IgG2a Production In Vivo of September 24, 2021. Birinder Ghumman, Edward M. Bertram and Tania H. Watts J Immunol 1998; 161:3262-3270; ; http://www.jimmunol.org/content/161/7/3262 Downloaded from References This article cites 44 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/161/7/3262.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 24, 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. Chemical Chaperones Enhance Superantigen and Conventional Antigen Presentation by HLA-DM-Deficient as well as HLA-DM-Sufficient Antigen-Presenting Cells and Enhance IgG2a Production In Vivo1 Birinder Ghumman, Edward M. Bertram, and Tania H. Watts2 Chemical chaperones, first defined in studies of mutant cystic fibrosis transmembrane conductance regulator proteins, are small molecules that act as stabilizers of proteins in their native state and have the ability in some cases to rescue protein-folding mutants within cells. HLA-DM is an MHC II-specific molecular chaperone that facilitates peptide loading onto MHC II proteins and also stabilizes empty MHC II molecules prior to their acquisition of antigenic peptides. APC that lack HLA-DM exhibit quantitative Downloaded from defects in protein Ag as well as superantigen presentation. Here we show that both the superantigen and protein presentation defect in MHC II-transfected, HLA-DM-deficient T2 cells can be partially overcome by treating the APC with the chemical chaperones glycerol, DMSO, or trimethylamine oxide. These chemical chaperones also enhance superantigen and conventional Ag presentation by wild-type APC. In vivo, glycerol was found to act as an adjuvant and resulted in enhanced IgG2a production to trinitrophenyl-keyhole limpet hemocyanin (TNP-KLH). In vitro, the enhancement of Ag presentation by chemical chaperones was found to take place at the level of the APC and took several hours to develop. Subcellular fractionation experiments show that http://www.jimmunol.org/ HLA-DM enhances presentation of peptides by dense endosome fractions whereas chemical chaperones enhance presentation by light membrane fractions (early endosome or plasma membrane). The mechanism by which these chemical chaperones augment Ag presentation is not defined, but flow cytometric analysis suggests that the enhancement may be due to a subtle effect on the stability of several different proteins at the cell surface. The Journal of Immunology, 1998, 161: 3262–3270. olecular chaperones bind to non-native conformations heterodimers on an invariant trimer (3). In the absence of invariant of proteins and stabilize them against irreversible ag- chain, MHC II is poorly expressed and largely remains aggregated gregation. Through controlled cycles of binding and in the ER (4–6). Thus, invariant chain is considered to be a spe- M by guest on September 24, 2021 release, molecular chaperones can facilitate the protein-folding cific molecular chaperone of the MHC II biosynthetic pathway. process. Once the native conformation of a protein is achieved, After assembly in the ER, the nonomeric abIi complex travels molecular chaperones no longer bind. Thus, molecular chaperones via the Golgi to an endocytic compartment where invariant chain are important in the retention of misfolded proteins as well as in is removed by proteolysis, leaving an MHC II a/b complex bound the protein-folding process itself (1). to a fragment of invariant chain, class II associate invariant chain The assembly of MHC class II molecules with their peptide peptides, CLIP (7, 8). In the endosome, abCLIP or larger precur- ligands involves a complex biosynthetic pathway in which molec- sors are acted upon by another specialized molecular chaperone, ular chaperones are involved at several stages (2). Shortly after HLA-DM. HLA-DM binds to MHC II molecules and thereby fa- synthesis in the endoplasmic reticulum (ER),3 individual MHC a- cilitates release of CLIP and other unstably bound peptides from and b-chains associate with the molecular chaperone calnexin. MHC II molecules (9–19). In addition, HLA-DM can stabilize Heterodimers of MHC II a- and b-chains are then assembled upon empty MHC II dimers and therefore maintain them in a state suit- an invariant chain (Ii) trimer that also contains bound calnexin. able for peptide binding, hence its definition as a molecular Calnexin dissociates from the Ii-MHC a/b complex upon comple- chaperone (20, 21). tion of formation of a nonameric complex consisting of three a/b APC that lack HLA-DM have a defect in peptide loading within APC (22). MHC II molecules in these cells remain associated with CLIP (23, 24). MHC II-CLIP complexes differ in kinetic stability Department of Immunology, University of Toronto, Toronto, Ontario, Canada from mature MHC II molecules as reflected in the instability of the Received for publication September 5, 1997. Accepted for publication May 27, 1998. CLIP-occupied MHC II dimer to SDS, at least for some MHC II The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance alleles (16, 22). HLA-DM-deficient APC present native protein with 18 U.S.C. Section 1734 solely to indicate this fact. Ags poorly (22, 25). However, HLA-DM deficiency does not im- 1 This work was supported by a grant from the National Cancer Institute of Canada pair surface expression of class II; therefore, DM-deficient cells (T.H.W.) with funds from the Terry Fox Foundation. T.H.W. is a senior research are capable of peptide presentation at the cell surface (22, 25). The scientist of the National Cancer Institute of Canada. affinity of CLIP for different MHC II alleles is quite variable, with 2 Address correspondence and reprint requests to Dr. Tania H. Watts, Department of k Immunology, University of Toronto, Toronto, ON M5S 1A8, Canada. E-mail address: that for A being particularly low (26, 27). As a result, HLA-DM- k [email protected] deficient cells express A in the SDS-stable, CLIP-unoccupied 3 Abbreviations used in this paper: ER, endoplasmic reticulum; CLIP, class II asso- form, and the Ag presentation defect is not as severe as in DM- ciate invariant chain peptides; TMAO, trimethylamine oxide; CFTR, cystic fibrosis deficient cells expressing other MHC II alleles (28). However, in transmembrane conductance regulator protein; SEA, staphylococcal enterotoxin A; k PE, phycoerythrin; HB, homogenization buffer; HEL, hen egg lysozyme; KLH, key- the absence of HLA-DM, T cells specific for A and HEL46-61 hole limpet hemocyanin; TNP, trinitrophenyl. respond poorly to hen egg lysozyme (HEL) protein processed Copyright © 1998 by The American Association of Immunologists 0022-1767/98/$02.00 The Journal of Immunology 3263 within the APC (25) a defect that can be corrected, at least in part, tario, Canada) and 500 ng/ml Puromycin (Sigma, St. Louis, MO). SEA was by HLA-DM transfection (29). purchased from Toxin Technology (Sarasota, FL). Synthetic HEL46-61 In addition to an effect on protein Ag presentation, HLA-DM- was purchased from the Ontario Cancer Institute Biotechnology Facility (Toronto, Canada). The anti-Ak-producing hybridomas 10-2.16 and 11-5.2 deficient cells have a defect in presentation of the superantigen were obtained from the American Type Culture Collection. The anti-Aak- staphylococcal enterotoxin A (SEA) by murine MHC II molecules producing hybridoma 39J (41) was kindly provided by W. Wade (Dart- (30, 31). The staphylococcal enterotoxins are 25-kDa proteins that mouth Medical School, Hanover, NH). Abs were purified from hybridoma bind as intact proteins to MHC II proteins outside the peptide- culture supernatants using protein A or G Sepharose (Pharmacia, Piscat- away, NJ). For biotinylation, Abs were dialyzed overnight against 0.1 M binding groove and activate T cells by simultaneously binding to sodium bicarbonate, pH 8.5, followed by incubation with a 10-fold molar the MHC II on the APC and the TCR on T cells expressing par- excess of N-hydroxysuccinimidyl-D-biotin for2hatroom temperature. ticular TCR Vb segments (reviewed in Ref. 32). The binding of Free biotin was removed by dialysis against PBS. The superantigen SEA SEA to MHC II is peptide dependent, and the affinity of this toxin was biotinylated by the same method using a 10- or 20-fold molar excess for MHC II varies greatly with the peptide bound in the groove of N-hydroxysuccinimidyl-D-biotin over SEA. (33). Indeed, SEA does not appear to be presented efficiently by Treatment of APC with chemical chaperones and b CLIP-occupied A expressed on HLA-DM-deficient T2 cells (30). Ag/superantigen presentation assays Although not exclusively occupied with CLIP (28, 31), Ak mole- cules expressed on HLA-DM-deficient T2 cells also show a quan- The chemical chaperones DMSO, glycerol (BDH, Analar quality, distrib- uted by VWR Scientific, Mississauga, Canada), and TMAO (Sigma) were titative defect in their ability to bind and present SEA, a defect that diluted in serum-free culture medium and added to the cells at the con- is corrected by HLA-DM transfection (31).
Load more

Recommended publications
  • Systematic Examination of Antigen-Specific Recall T Cell
    Systematic Examination of Antigen-Specific Recall T Cell Responses to SARS-CoV-2 versus Influenza Virus Reveals a Distinct Inflammatory Profile This information is current as of November 24, 2020. Jaclyn C. Law, Wan Hon Koh, Patrick Budylowski, Jonah Lin, FengYun Yue, Kento T. Abe, Bhavisha Rathod, Melanie Girard, Zhijie Li, James M. Rini, Samira Mubareka, Allison McGeer, Adrienne K. Chan, Anne-Claude Gingras, Tania H. Watts and Mario A. Ostrowski Downloaded from J Immunol published online 18 November 2020 http://www.jimmunol.org/content/early/2020/11/17/jimmun ol.2001067 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2020/11/17/jimmunol.200106 Material 7.DCSupplemental Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision by guest on November 24, 2020 • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Author Choice Freely available online through The Journal of Immunology Author Choice option 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. Published November 18, 2020, doi:10.4049/jimmunol.2001067 The Journal of Immunology Systematic Examination of Antigen-Specific Recall T Cell Responses to SARS-CoV-2 versus Influenza Virus Reveals a Distinct Inflammatory Profile Jaclyn C.
    [Show full text]
  • Dr. Tania Watts
    Interviews Interview with an Immunologist: Dr. Tania Watts Dario M. Ferri and Luke S. Dingwell r. Tania Watts received her After the initial shock dissipated, I started to think Well,“ Ph.D. in Biochemistry from we’re experts in viral immunology, we should do something” - the University of Alberta. She fortunately, I have colleagues in Dr. Mario Ostrowski and Dr. Dthen went on to do a post-doctoral Allison McGeer, both infectious diseases clinician scientists, fellowship at Stanford University so I reached out to them about the possibility of setting up studying T lymphocyte activation, which a project focused on studying human T cell responses to is where she first began to develop her SARS-CoV-2. Once we finalized our idea for the project, passion for immunology. During her there was a bit of a scramble to get all of the necessary post-doctoral work, Dr. Watts helped biosafety approval, but we began our work on SARS-CoV-2 to provide the first evidence for the immunity. I am very fortunate to have an extremely smart existence of a ternary complex existing and hardworking PhD student in Jaclyn Law, who in the between MHC II, peptide antigen, and past few months has had to completely pivot her PhD thesis Dr. Tania Watts the T cell receptor. In 1986, Dr. Watts work towards focusing on SARS-CoV-2 immunity. It was took up a faculty position at the University of Toronto Department also a very active collaboration with members of Mario of Immunology, where her research has been focused on T cell and Ostrowski’s team contributing their assays and expertise as viral immunity.
    [Show full text]
  • And CD137L Responses by Dual Costimulation with CD80
    Enhancement of HIV-Specific CD8 T Cell Responses by Dual Costimulation with CD80 and CD137L This information is current as Jacob Bukczynski, Tao Wen, Chao Wang, Natasha Christie, of September 28, 2021. Jean-Pierre Routy, Mohamed-Rachid Boulassel, Colin M. Kovacs, Kelly S. MacDonald, Mario Ostrowski, Rafick-Pierre Sekaly, Nicole F. Bernard and Tania H. Watts J Immunol 2005; 175:6378-6389; ; doi: 10.4049/jimmunol.175.10.6378 Downloaded from http://www.jimmunol.org/content/175/10/6378 References This article cites 57 articles, 30 of which you can access for free at: http://www.jimmunol.org/content/175/10/6378.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 28, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2005 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Enhancement of HIV-Specific CD8 T Cell Responses by Dual Costimulation with CD80 and CD137L1 Jacob Bukczynski,* Tao Wen,2* Chao Wang,* Natasha Christie,* Jean-Pierre Routy,† Mohamed-Rachid Boulassel,† Colin M.
    [Show full text]
  • Imm250h1f “Immunity and Infection” – Fall 2016
    IMM250H1F “IMMUNITY AND INFECTION” – FALL 2016 Students will be introduced to the basic concepts of immunity to infectious disease. We will trace the history of current ideas in immunology by examining how bacteria and viruses cause disease and the initial discoveries that led to such developments as vaccination. Current topical and newsworthy infectious diseases (HIV, Ebola, avian flu, Sepsis) will be used as examples of how the immune system copes with microbial infections and how breakdown of the immune response can lead to diseases such as autoimmunity. IMM250 is a required course for all immunology programs, however it is designed to fulfill breadth requirements and is an appropriate choice for students in other science or humanities programs. Development of writing skills through the composition of a science article for the general public is one objective of this course. Recommended Preparation: BIO120H, BIO130H COURSE DATES AND POLICIES Class time: Tuesdays, 10AM-12noon, Location: OISE Auditorium room G162, 252 Bloor Street. Course coordinator: Dr. Liliana Clemenza [email protected] All postings (lecture material and announcements) will be done on Blackboard. Please check the Portal regularly. Lecturers: Dr. L. Clemenza Office hours: Mondays 12:30-2:30pm, room MSB 7267. Please email in advance for appointment. Other meeting arrangements can be made upon request. Dr. Wendy Tamminen [email protected] Office hours: TBA Guest Lecturers: Dr. Tania Watts Dr. Brian Barber 1 Evaluation Summary and Event Dates: 1. Midterm Test: Weight 20% (multiple-choice questions), it will include the first 5 lectures. When: Tuesday October 11 2016, 11am-12noon (one hour) Location: Exam Centre, rooms: TBA, 255 McCaul Street.
    [Show full text]
  • GITRL on Inflammatory Antigen Presenting Cells in the Lung
    www.nature.com/mi ARTICLE GITRL on inflammatory antigen presenting cells in the lung parenchyma provides signal 4 for T-cell accumulation and tissue-resident memory T-cell formation Kuan-Lun Chu1, Nathalia V. Batista1, Kuan Chung Wang1, Angela C. Zhou1 and Tania H. Watts1 T-cell responses in the lung are critical for protection against respiratory pathogens. TNFR superfamily members play important roles in providing survival signals to T cells during respiratory infections. However, whether these signals take place mainly during priming in the secondary lymphoid organs and/or in the peripheral tissues remains unknown. Here we show that under conditions of competition, GITR provides a T-cell intrinsic advantage to both CD4 and CD8 effector T cells in the lung tissue, as well as for the formation of CD4 and CD8 tissue-resident memory T cells during respiratory influenza infection in mice. In contrast, under non- competitive conditions, GITR has a preferential effect on CD8 over CD4 T cells. The nucleoprotein-specific CD8 T-cell response partially compensated for GITR deficiency by expansion of higher affinity T cells; whereas, the polymerase-specific response was less flexible and more GITR dependent. Following influenza infection, GITR is expressed on lung T cells and GITRL is preferentially expressed on lung monocyte-derived inflammatory antigen presenting cells. Accordingly, we show that GITR+/+ T cells in the lung parenchyma express more phosphorylated-ribosomal protein S6 than their GITR−/− counterparts. Thus, GITR signaling within the lung tissue critically regulates effector and tissue-resident memory T-cell accumulation. Mucosal Immunology (2019) 12:363–377; https://doi.org/10.1038/s41385-018-0105-5 INTRODUCTION checkpoint for CD4 accumulation and shows only indirect effects Influenza remains an important human pathogen.
    [Show full text]
  • October/November 2018
    Department of Immunology Newsletter VOL VII – ISSUE 2 October/November 2018 Message from the Chair, UPCOMING EASTON SEMINARS Dr. Juan Carlos Zúñiga-Pflücker November 2018 With fall fully upon us and with the main MSB 2172 at 11:10 a.m. grant-writing season finally over, it is a good time to start thinking about upcoming events in the Monday, November 5 Department of Immunology. With this in mind, Dr. Graham Pawelec, PhD please note the save the date(s) section. "Interplay between Age, Immunity, Cancer and I am also looking forward to our next departmental CMV" faculty meeting, during which I will provide an Host: Dr. Tania Watts, PhD overview of the next strategic plan for our department. This new plan will be the 2nd Strategic Monday, November 12 Plan for the department, and will build on the many Dr. Alan Sher, PhD successes achieved from our initial strategic plan "Iron Dependent Targets for Host-Directed (2014-2018). In the meantime, we will be Therapy of TB" Host: Dr. David Brooks, PhD conducting interviews and discussion with many of our stakeholders and external advisors to ensure Monday, November 19 our plan reflects areas that still need improvement Dr. Michael Gold, PhD and highlights those that can be further developed. "B Cell Activation in Space and Time" I am also taking this opportunity to say that all look Host: Dr. Robert Rottapel, MD forward to hearing from all of you regarding any new ideas and/or advice that be included as part of Monday, November 26 —No Easton Seminar our new plan.
    [Show full text]
  • A Critical Role for TNF Receptor-Associated Factor 1 and Bim Down-Regulation in CD8 Memory T Cell Survival
    A critical role for TNF receptor-associated factor 1 and Bim down-regulation in CD8 memory T cell survival Laurent Sabbagh*, Cathy C. Srokowski*, Gayle Pulle*, Laura M. Snell*, Bradley J. Sedgmen*, Yuanqing Liu*, Erdyni N. Tsitsikov†, and Tania H. Watts*‡ *Department of Immunology, University of Toronto, 1 King’s College Circle, Toronto, ON, Canada M5S 1A8; and †CBR Institute for Biomedical Research, Harvard Medical School, WAB 124, 200 Longwood Avenue, Boston, MA 02468 Edited by Philippa Marrack, National Jewish Medical and Research Center, Denver, CO, and approved October 16, 2006 (received for review April 10, 2006) The mechanisms that allow the maintenance of immunological involved in the promotion as well as feedback inhibition of TRAF2- memory remain incompletely defined. Here we report that tumor mediated signaling events. necrosis factor receptor (TNFR)-associated factor (TRAF) 1, a protein In T cells, TRAF1 deficiency results in hyperresponsiveness to recruited in response to several costimulatory TNFR family mem- anti-CD3 and TNF stimulation in vitro, suggesting that TRAF1 is bers, is required for maximal CD8 T cell responses to influenza virus a negative regulator of T cell activation (14). In contrast, constitu- in mice. Decreased recovery of CD8 T cells in vivo occurred under tive overexpression of a TRAF1 transgene in a T cell antigen conditions where cell division was unimpaired. In vitro, TRAF1- receptor (TCR) transgenic model led to reduced antigen-induced deficient, antigen-activated T cells accumulated higher levels of the cell death (15). However, the effect of TRAF1 deficiency on proapoptotic BH3-only family member Bim, particularly the most antigen-specific T cell responses in vivo has not yet been analyzed.
    [Show full text]
  • Recent Advances in Immunology IMM1000Y-Syllabus
    Recent Advances in Immunology IMM1000Y Date/Time: Mondays 1:30-4:00pm (unless otherwise specified) Location: Health Science Building – Room 108 155 College Street TORONTO, ON, Canada M5T 1P8 Room 108 is a tentative location reserved for dates that will allow in-person lectures. Under the current circumstances lectures and student presentations will be held in an online, synchronous format (Mondays, 1:30-4:00pm). An invitation to a Zoom meeting will be provided by the course coordinator for each lecture. Note that lectures and student presentations will not be recorded. Course coordinator: Arthur Mortha ([email protected]) Please note that students who are not in the graduate program in Immunology need to obtain prior permission from the course coordinator to register for this course. Prerequisite: The prerequisite for this course is a basic background in Immunology obtained from at least one recent full-year undergraduate course. The course will be taught at a fairly advanced level. Students who are missing background knowledge in some areas should fill the gaps from textbook, discussions with colleagues, or advice from faculty members. Don’t hesitate to reach out. Recommended textbook: Primer to The Immune Response, 2nd Edition. Tak W. Mak, Mary Saunders, and Bradley Jett. 2014 (Academic Press). Evaluation Scheme & Course Assessments: Assessment % of Grade Due Date Midterm Exam 35% December 11, 2020 (4:00pm) Presentation 20% Throughout term Final Exam 45% March 29, 2021 (4:00pm) *All grading will be done by the professor/s who submitted the question or assigned the paper for presentation. The course coordinator will assemble the marks and administer the final mark.
    [Show full text]
  • L and Bcl-X Staying Alive
    Staying Alive: T Cell Costimulation, CD28, and Bcl-x L Tania H. Watts This information is current as J Immunol 2010; 185:3785-3787; ; of September 25, 2021. doi: 10.4049/jimmunol.1090085 http://www.jimmunol.org/content/185/7/3785 Downloaded from References This article cites 39 articles, 20 of which you can access for free at: http://www.jimmunol.org/content/185/7/3785.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 25, 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 © 2010 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Staying Alive: T Cell Costimulation, CD28, and Bcl-xL Tania H. Watts he survival of lymphocytes is tightly regulated at each cemented the role of CD28 as a key receptor for signal 2 for stage of their lifespan. Although this may seem ob- T lymphocyte activation (14–19). T vious to us today, prior to the early 1990s, the focus of At the time of the studies of Boise et al.
    [Show full text]
  • Chronic Viral Infection in Mice Ligand Expression on APC Subsets Over
    Conserved and Differential Features of TNF Superfamily Ligand Expression on APC Subsets over the Course of a Chronic Viral Infection in Mice Kuan C. Wang, Kuan-Lun Chu, Nathalia V. Batista and Tania H. Watts Downloaded from ImmunoHorizons 2018, 2 (11) 407-417 doi: https://doi.org/10.4049/immunohorizons.1800047 http://www.immunohorizons.org/content/2/11/407 http://www.immunohorizons.org/ This information is current as of October 3, 2021. Supplementary http://www.immunohorizons.org/content/suppl/2018/12/20/2.11.407.DCSup Material plemental References This article cites 33 articles, 10 of which you can access for free at: http://www.immunohorizons.org/content/2/11/407.full#ref-list-1 Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: by guest on October 3, 2021 http://www.immunohorizons.org/alerts ImmunoHorizons is an open access journal published by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 All rights reserved. ISSN 2573-7732. RESEARCH ARTICLE Infectious Disease Conserved and Differential Features of TNF Superfamily Ligand Expression on APC Subsets over the Course of a Chronic Viral Infection in Mice Kuan C. Wang, Kuan-Lun Chu, Nathalia V. Batista, and Tania H. Watts Downloaded from Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada ABSTRACT http://www.immunohorizons.org/ There is currently much interest in how different APC subsets shape the immune response. We recently described a division of labor between classical dendritic cells (cDC) and inflammatory monocyte-derived APC in provision of costimulatory ligands to T cells early during chronic lymphocytic choriomeningitis clone 13 (LCMV 13) infection in mice.
    [Show full text]
  • 2017-2018 Immunology Seminar Series 12:00 – 1:00 PM, Scaife Auditorium 5 Contact: Jesse Rosenthal, [email protected], 412-648-7050
    2017-2018 Immunology Seminar Series 12:00 – 1:00 PM, Scaife Auditorium 5 Contact: Jesse Rosenthal, [email protected], 412-648-7050 SEPTEMBER 7 – Wajahat Mehal, MD, PhD, Yale University “Sterile Inflammation in the Liver” 14 – Geoffrey Camirand, PhD, University of Pittsburgh “Visualization of Treg suppressor function within non-lymphoid tissues” 21 – NO SEMINAR – Rosh Hoshanah 28 – NO SEMINAR – Department Retreat OCTOBER 5 – EBERLY LECTURE – Klaus Rajewsky, MD, Max Delbruck Center for Molecular Medicine “Signals Controlling Normal and Malignant B Cells” 12 – Charles Drake, MD, PhD, Columbia University “Immunotherapy for GU Cancers” 19 – NO SEMINAR – Science 2017 26 – Shruti Naik, MD, Rockefeller University “Memory of Inflammation in Epidermal Stem Cells” NOVEMBER 2 – Mike Rosenblum, MD, PhD, University of California, San Francisco “Regulatory T Cells in Skin – From Mice to Man” 9 – NO SEMINAR 16 – Robert Lafyatis, MD, University of Pittsburgh “Expansion of pro-fibrotic fibroblasts and macrophages in idiopathic pulmonary fibrosis” 23 – NO SEMINAR – THANKSGIVING 30 – Eugene Oltz, PhD, Washington University in St. Louis “Normal and Pathogenic Regulatory Circuits Governing Gene Expression in Human Lymphoid Cells” DECEMBER 7 – Michael Cancro, PhD, University of Pennsylvania “New subsets, new checkpoints: Expanding roles for Tbet+ B cells in health and disease” 14 – Greg Delgoffe, PhD, University of Pittsburgh 2017-2018 Immunology Seminar Series 12:00 – 1:00 PM, Scaife Auditorium 5 Contact: Jesse Rosenthal, [email protected], 412-648-7050
    [Show full text]
  • Chronic Viral Infection in Mice Ligand Expression on APC Subsets Over
    Conserved and Differential Features of TNF Superfamily Ligand Expression on APC Subsets over the Course of a Chronic Viral Infection in Mice Kuan C. Wang, Kuan-Lun Chu, Nathalia V. Batista and Tania H. Watts Downloaded from ImmunoHorizons 2018, 2 (11) 407-417 doi: https://doi.org/10.4049/immunohorizons.1800047 http://www.immunohorizons.org/content/2/11/407 http://www.immunohorizons.org/ This information is current as of October 6, 2021. Supplementary http://www.immunohorizons.org/content/suppl/2018/12/20/2.11.407.DCSup Material plemental References This article cites 33 articles, 10 of which you can access for free at: http://www.immunohorizons.org/content/2/11/407.full#ref-list-1 Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: by guest on October 6, 2021 http://www.immunohorizons.org/alerts ImmunoHorizons is an open access journal published by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 All rights reserved. ISSN 2573-7732. RESEARCH ARTICLE Infectious Disease Conserved and Differential Features of TNF Superfamily Ligand Expression on APC Subsets over the Course of a Chronic Viral Infection in Mice Kuan C. Wang, Kuan-Lun Chu, Nathalia V. Batista, and Tania H. Watts Downloaded from Department of Immunology, University of Toronto, Toronto, Ontario M5S 1A8, Canada ABSTRACT http://www.immunohorizons.org/ There is currently much interest in how different APC subsets shape the immune response. We recently described a division of labor between classical dendritic cells (cDC) and inflammatory monocyte-derived APC in provision of costimulatory ligands to T cells early during chronic lymphocytic choriomeningitis clone 13 (LCMV 13) infection in mice.
    [Show full text]