Acquired Immunity
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The Evelyn F. and William L. Mcknight Brain Institute and the Cognitive Aging and Memory – Clinical Translational Research Program (CAM-CTRP) 2015 Annual Report
The Evelyn F. and William L. McKnight Brain Institute and the Cognitive Aging and Memory – Clinical Translational Research Program (CAM-CTRP) 2015 Annual Report Prepared for the McKnight Brain Research Foundation by the University of Florida McKnight Brain Institute and Institute on Aging Table of Contents Letter from UF Leadership ................................................................................................................................................................................................. 3 Age-related Memory Loss (ARML) Program and the Evelyn F. McKnight Chair for Brain Research in Memory Loss...... 4-19 Cognitive Aging and Memory Clinical Translational Research Program (CAM-CTRP) and the Evelyn F. McKnight Chair for Clinical Translational Research in Cognitive Aging and Memory ................................ 20-63 William G. Luttge Lectureship in Neuroscience ...............................................................................................................64-65 Program Financials .................................................................................................................................................................. 66 Age-related Memory Loss Program .............................................................................................................................................................................67 McKnight Endowed Chair for Brain Research in Memory Loss .........................................................................................................................68 -
LECTURE 05 Acquired Immunity and Clonal Selection
LECTURE: 05 Title: ACQUIRED "ADAPTIVE" IMMUNITY & CLONAL SELECTION THEROY LEARNING OBJECTIVES: The student should be able to: • Recognize that, acquired or adaptive immunity is a specific immunity. • Explain the mechanism of development of the specific immunity. • Enumerate the components of the specific immunity such as A. Primary immune response. B. Secondary immune response • Explain the different phases that are included in the primary and secondary immune responses such as: A. The induction phase. B. Exponential phase. C. Steady phase. D. Decline phase. • Compare between the phases of the primary and secondary immune responses. • Determine the type of the immunoglobulins involved in each phase. • Determine which immunoglobulin is induced first and, that last longer. • Enumerate the characteristics of the specific immunity such as: A. The ability to distinguish self from non-self. B. Specificity. C. Immunological memory. • Explain naturally and artificially acquired immunity (passive, and active). • Explain the two interrelated and independent mechanisms of the specific immune response such as : A. Humoral immunity. B. Cell-mediated (cellular) immunity. • Recognize that, the specific immunity is not always protective, for example; sometimes it causes allergies (hay fever), or it may be directed against one of the body’s own constituents, resulting in autoimmunity (thyroditis). LECTURE REFRENCE: 1. TEXTBOOK: ROITT, BROSTOFF, MALE IMMUNOLOGY. 6th edition. Chapter 2. pp. 15-31 2. TEXTBOOK: ABUL K. ABBAS. ANDREW H. LICHTMAN. CELLULAR AND MOLECULAR IMMUNOLOGY. 5TH EDITION. Chapter 1. pg 3-12. 1 ACQUIRED (SPECIFIC) IMMUNITY INTRODUCTION Adaptive immunity is created after an interaction of lymphocytes with particular foreign substances which are recognized specifically by those lymphocytes. -
The Dichotomous Role of Inflammation in The
biomolecules Review The Dichotomous Role of Inflammation in the CNS: A Mitochondrial Point of View Bianca Vezzani 1,2 , Marianna Carinci 1,2 , Simone Patergnani 1,2 , Matteo P. Pasquin 1,2, Annunziata Guarino 2,3, Nimra Aziz 2,3, Paolo Pinton 1,2,4, Michele Simonato 2,3,5 and Carlotta Giorgi 1,2,* 1 Department of Medical Sciences, University of Ferrara, 44121 Ferrara, Italy; [email protected] (B.V.); [email protected] (M.C.); [email protected] (S.P.); [email protected] (M.P.P.); [email protected] (P.P.) 2 Laboratory of Technologies for Advanced Therapy (LTTA), Technopole of Ferrara, 44121 Ferrara, Italy; [email protected] (A.G.); [email protected] (N.A.); [email protected] (M.S.) 3 Department of BioMedical and Specialist Surgical Sciences, University of Ferrara, 44121 Ferrara, Italy 4 Maria Cecilia Hospital, GVM Care & Research, 48033 Cotignola (RA), Italy 5 School of Medicine, University Vita-Salute San Raffaele, 20132 Milan, Italy * Correspondence: [email protected]; Tel.: +39-0532-455803 Received: 28 August 2020; Accepted: 10 October 2020; Published: 13 October 2020 Abstract: Innate immune response is one of our primary defenses against pathogens infection, although, if dysregulated, it represents the leading cause of chronic tissue inflammation. This dualism is even more present in the central nervous system, where neuroinflammation is both important for the activation of reparatory mechanisms and, at the same time, leads to the release of detrimental factors that induce neurons loss. Key players in modulating the neuroinflammatory response are mitochondria. Indeed, they are responsible for a variety of cell mechanisms that control tissue homeostasis, such as autophagy, apoptosis, energy production, and also inflammation. -
The CNS and the Brain Tumor Microenvironment: Implications for Glioblastoma Immunotherapy
International Journal of Molecular Sciences Review The CNS and the Brain Tumor Microenvironment: Implications for Glioblastoma Immunotherapy Fiona A. Desland and Adília Hormigo * Icahn School of Medicine at Mount Sinai, The Tisch Cancer Institute, Department of Neurology, Box 1137, 1 Gustave L. Levy Pl, New York, NY 10029-6574, USA; fi[email protected] * Correspondence: [email protected] Received: 28 August 2020; Accepted: 29 September 2020; Published: 5 October 2020 Abstract: Glioblastoma (GBM) is the most common and aggressive malignant primary brain tumor in adults. Its aggressive nature is attributed partly to its deeply invasive margins, its molecular and cellular heterogeneity, and uniquely tolerant site of origin—the brain. The immunosuppressive central nervous system (CNS) and GBM microenvironments are significant obstacles to generating an effective and long-lasting anti-tumoral response, as evidenced by this tumor’s reduced rate of treatment response and high probability of recurrence. Immunotherapy has revolutionized patients’ outcomes across many cancers and may open new avenues for patients with GBM. There is now a range of immunotherapeutic strategies being tested in patients with GBM that target both the innate and adaptive immune compartment. These strategies include antibodies that re-educate tumor macrophages, vaccines that introduce tumor-specific dendritic cells, checkpoint molecule inhibition, engineered T cells, and proteins that help T cells engage directly with tumor cells. Despite this, there is still much ground to be gained in improving the response rates of the various immunotherapies currently being trialed. Through historical and contemporary studies, we examine the fundamentals of CNS immunity that shape how to approach immune modulation in GBM, including the now revamped concept of CNS privilege. -
PTSD Is Associated with Neuroimmune Suppression: Evidence from PET Imaging and Postmortem Transcriptomic Studies
ARTICLE https://doi.org/10.1038/s41467-020-15930-5 OPEN PTSD is associated with neuroimmune suppression: evidence from PET imaging and postmortem transcriptomic studies Shivani Bhatt 1, Ansel T. Hillmer2,3,4, Matthew J. Girgenti 3,5, Aleksandra Rusowicz 3, Michael Kapinos4, Nabeel Nabulsi 2,4, Yiyun Huang2,4, David Matuskey 2,3,4, Gustavo A. Angarita3,4, Irina Esterlis1,3,4,5, Margaret T. Davis3, Steven M. Southwick3,5, Matthew J. Friedman 6, Traumatic Stress Brain Study Group*, Ronald S. Duman 3, Richard E. Carson 2,4, John H. Krystal3,5, Robert H. Pietrzak3,5 & ✉ Kelly P. Cosgrove 1,2,3,4,5 1234567890():,; Despite well-known peripheral immune activation in posttraumatic stress disorder (PTSD), there are no studies of brain immunologic regulation in individuals with PTSD. [11C]PBR28 Positron Emission Tomography brain imaging of the 18-kDa translocator protein (TSPO), a microglial biomarker, was conducted in 23 individuals with PTSD and 26 healthy individuals— with or without trauma exposure. Prefrontal-limbic TSPO availability in the PTSD group was negatively associated with PTSD symptom severity and was significantly lower than in controls. Higher C-reactive protein levels were also associated with lower prefrontal-limbic TSPO availability and PTSD severity. An independent postmortem study found no differential gene expression in 22 PTSD vs. 22 controls, but showed lower relative expression of TSPO and microglia-associated genes TNFRSF14 and TSPOAP1 in a female PTSD subgroup. These findings suggest that peripheral immune activation in PTSD is associated with deficient brain microglial activation, challenging prevailing hypotheses positing neuroimmune activation as central to stress-related pathophysiology. -
Vaccine Immunology Claire-Anne Siegrist
2 Vaccine Immunology Claire-Anne Siegrist To generate vaccine-mediated protection is a complex chal- non–antigen-specifc responses possibly leading to allergy, lenge. Currently available vaccines have largely been devel- autoimmunity, or even premature death—are being raised. oped empirically, with little or no understanding of how they Certain “off-targets effects” of vaccines have also been recog- activate the immune system. Their early protective effcacy is nized and call for studies to quantify their impact and identify primarily conferred by the induction of antigen-specifc anti- the mechanisms at play. The objective of this chapter is to bodies (Box 2.1). However, there is more to antibody- extract from the complex and rapidly evolving feld of immu- mediated protection than the peak of vaccine-induced nology the main concepts that are useful to better address antibody titers. The quality of such antibodies (e.g., their these important questions. avidity, specifcity, or neutralizing capacity) has been identi- fed as a determining factor in effcacy. Long-term protection HOW DO VACCINES MEDIATE PROTECTION? requires the persistence of vaccine antibodies above protective thresholds and/or the maintenance of immune memory cells Vaccines protect by inducing effector mechanisms (cells or capable of rapid and effective reactivation with subsequent molecules) capable of rapidly controlling replicating patho- microbial exposure. The determinants of immune memory gens or inactivating their toxic components. Vaccine-induced induction, as well as the relative contribution of persisting immune effectors (Table 2.1) are essentially antibodies— antibodies and of immune memory to protection against spe- produced by B lymphocytes—capable of binding specifcally cifc diseases, are essential parameters of long-term vaccine to a toxin or a pathogen.2 Other potential effectors are cyto- effcacy. -
P:\Autism Cases\Dwyer 03-1202V\Opinion Segments NEW
IN THE UNITED STATES COURT OF FEDERAL CLAIMS OFFICE OF THE SPECIAL MASTERS No. 03-1202V Filed: March 12, 2010 ******************************************************* TIMOTHY and MARIA DWYER, parents of * COLIN R. DWYER, a minor, * Omnibus Autism Proceeding; * Theory 2 Test Case; Petitioners, * Thimerosal-Containing Vaccines; * Ethylmercury; Causation; v. * “Clearly Regressive” Autism; * Oxidative Stress; Sulfur SECRETARY OF THE DEPARTMENT OF * Metabolism Disruption; HEALTH AND HUMAN SERVICES, * Excitotoxicity; Expert * Qualifications; Weight of the Respondent. * Evidence * ******************************************************* DECISION1 James Collins Ferrell, Esq., Houston, TX; Thomas B. Powers, Esq. and Michael L. Williams, Esq., Portland, OR; for petitioners. Lynn Elizabeth Ricciardella, Esq. and Voris Johnson, Esq., U.S. Department of Justice, Washington, DC, for respondent. VOWELL, Special Master: On May 14, 2003, Timothy and Maria Dwyer [“petitioners”] filed a “short form” petition for compensation under the National Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-10, et seq.2 [the “Vaccine Act” or “Program”], on behalf of their minor 1 Vaccine Rule 18(b) provides the parties 14 days to request redaction of any material “(i) which is trade secret or commercial or financial information which is privileged and confidential, or (ii) which are medical files and similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.” 42 U.S.C § 300aa12(d)(4)(B). Both parties have waived their right to request such redaction. See Petitioners’ Notice to Waive the 14-Day Waiting Period, filed February 1, 2010; Respondent’s Consent to Disclosure, filed January 13, 2010. Accordingly, this decision will be publically available upon filing. 2 National Childhood Vaccine Injury Act of 1986, Pub. -
Humoral Immunity and Complement Humoral Immunity B Cell Antigens
Humoral Immunity Humoral Immunity and Complement Transfer of non-cell components of blood-- Robert Beatty antibodies, complement MCB150 Humoral immunity = antibody mediated B Cell Activation of T-dependent antigens B cell Antigens T cell dependent B cell antigens T cell independent Majority of antigens. Do not require thymus. Most protein antigens. No memory. T cell help required for B cell activation and antibody production. T-cell dependent antigens T-cell independent antigens 1 B Cell Activation T-dependent antigens Location of B Cell Activation Antigen activated B cells remain in T cell zones of LN. Linked Recognition Maximize contact of Need T cell epitope along with B cell epitope to B cells with T cells. get antibody response. B cells get help from T cells, help = CD40Ligand and IL-4. Clonal proliferation In Follicles Isotype Switching Affinity maturation Somatic hypermutation 2 T cell Independent Antigens B cell mitogens (e.g. LPS) B-1 cells At low levels normal immune response to LPS Activated by repeating CHO epitopes that provide crosslinking At high levels LPS can cause non-antigen specific to induce antigen uptake and activation. activation of B cells. Mitogen effect Antigen specific immune response Lower affinity, lower numbers, no memory. Primarily IgM. Antibody Effector Functions Opsonization Neutralization Antibody Effector Functions Enhancement of phagocytosis Neutralizing abs block active site for adherence, entry into host cell, or active site of toxin Neutralizing antibodies are usually high affinity and primarily IgG. 3 Antibody-dependent cell-mediated Complement Activation cytotoxicity (ADCC) Antibody Effector Functions Antibody Effector Functions Antibody binds to pathogen or infected target cell. -
Cellular and Humoral Components of Monocyte and Neutrophil Chen1otaxis in Cord Blood
Pediat. Res. 11: 677-()1\0 (1977) Chemotaxis neutrophil complement newborn monocytes phagocytes Cellular and Humoral Components of Monocyte and Neutrophil Chen1otaxis in Cord Blood SAYITA G . PAHWA.""'' RAJENDRA PAHWA. ELENA GRII\IES. AND E LIZA13 ETII SI\IITII\VICK Departlllt'lll of Pediatrics aml/nmrwwlogy, Memorial Sloa/1-1\ellcrillg Ca11ca Centa, Nell' York, New York , USA Summary experiment, blood from a healthy adult was tested simultane ously. 1\lonoqte and polymorphonuclear neutrophil (J>I\IN) chemo taxis was studied in cord blood from healthv term infants. 1\Jono ISOLATION OF CELLS c;yte chemotaxis was normal to increased ( 115-126%) whereas PI\IN chemotaxis was decreased (79%) in comparison with that Mononuclear leukocytes were isolated by density gradient of healthy adult l'ontrol subjects. Generation of chemotactic centrifugation on a sodium mctrizoatc-Ficoll solution (Lympho factors from cord sera was impaired, being 55% of that gener prep. Nyegard and Co., Oslo) (5). The cells were washed three ated by J)(Wied normal human serum (I'NIIS). Cord serum was times and resuspended in RPI\11 (Gibco) supplemented with less inhibitory than pooled adult human serum fur adult mono penicillin 50 units, streptomycin 50 Jlg . and glutamine 2 ml\1/ml. qtes when the cells were suspended in HI % serum and tested for As simultaneous analysis of monocytcs by myelopcroxidasc stain chemotaxis. No inhibition of chemotactic factors by either cord and Wright stain were in close agreement. the percentage of or adult sera was observed. The dissociation of chemotactic monocytcs was routinely determined by a myelopcroxidasc stain response of the two diiTerent phagocytic cells may represent a ( 13 ); Wright stain was done to exclude contamination by gra nu protecth·e mechanism whereby one cell can compensate for a locytes. -
Autism and KIR Genes of the Human Genome: a Brief Meta-Analysis
The Egyptian Journal of Medical Human Genetics 19 (2018) 159–164 Contents lists available at ScienceDirect The Egyptian Journal of Medical Human Genetics journal homepage: www.sciencedirect.com Review Autism and KIR genes of the human genome: A brief meta-analysis Najmeh Pirzadroozbahani a, Seyyed Amir Yasin Ahmadi b, Hamidreza Hekmat c, Golnaz Atri Roozbahani d, ⇑ Farhad Shahsavar e, a Student Research Committee, Lorestan University of Medical Sciences, Khorramabad, Iran b Scientific Society of Evidence-based Knowledge, Research Office for the History of Persian Medicine, Lorestan University of Medical Sciences, Khorramabad, Iran c Department of Psychology, Islamic Azad University, Borujerd, Iran d Department of Life Science and Biotechnology, Shahid Beheshti University, Tehran, Iran e Department of Immunology, Hepatitis Research Center, Lorestan University of Medical Sciences, Khorramabad, Iran article info abstract Article history: Background: Killer cell immunoglobin-like receptors (KIR) are the transmembrane glycoproteins on nat- Received 4 October 2017 ural killer (NK) cells that regulate their functions. Studies show that immune system plays roles in neu- Accepted 29 October 2017 rodevelopmental disorders like autism, and NK cell abnormality can be a risk factor in autism spectrum Available online 6 November 2017 disorders. Aim: This study aims to investigate the role of KIR genes diversity in autism. Keywords: Methods: In order to find the relevant literature, we used PubMed, Google Scholar and other search Autism engines. Association of each gene was analyzed through chi-square with Yate’s correction (or Fisher’s Neuroimmunology exact test if necessary). Software comprehensive meta-analysis was used. Both fixed and random effect KIR NK cell models were reported. -
Developing Mind, Second Edition
Praise for THE DEVELOPING MIND “A tour de force of synthesis and integration. Siegel has woven a rich tapestry that provides a compelling account of how our interpersonal worlds and neural systems form two important pillars of the mind. The second edition brings the latest neuroscientific evidence to the fore; it is a ‘must read’ for any student or professional interested in mental health, child development, and the brain.” —RICHA R D J. DAVIDSON , PhD, William James and Vilas Professor of Psychology and Psychiatry; Founder and Chair, Center for Investigating Healthy Minds, University of Wisconsin–Madison “With the original publication of The Developing Mind, the field of interpersonal neurobiology was born. Siegel’s genius for synthesizing and humanizing neu- roscience, attachment, and developmental theory made the book a bestseller and attracted thousands to this new field. The second edition benefits from over a decade’s worth of additional findings, reflections, ideas, and insights. I encourage you to take Siegel up on his offer to share this fascinating journey, whether for the first time or for a return trip. You won’t be disappointed.” —LOUIS COZO L INO , PhD, Department of Psychology, Pepperdine University “When The Developing Mind was first published, Siegel’s proposal that mind, brain, and relationships represented ‘three aspects of one reality’ essential to human well-being still seemed closer to inspired speculation than teachable scientific knowledge. Just over a decade later, the neurobiology of interpersonal experience has grown into one of the hottest areas of psychological research. Over two thousand new references surveyed for the second edition testify to just how far neuroscientists, developmental psychologists, and clinicians have brought the field as they begin to more fully chart the interplay of mind, body, and relationships. -
Microbiota Gut-Brain Axis and Neurodegenerative Disease. a Systematic Review on Alzheimer’S Disease, Amyotrophic Lateral Sclerosis and Parkinson Disease
Microbiota Gut-Brain Axis and Neurodegenerative Disease. A systematic review on Alzheimer’s disease, Amyotrophic lateral sclerosis and Parkinson Disease Poluyi Edward Oluwatobi, Imaguezegie Grace Ese, Poluyi Abigail Oluwatumininu, Morgan Eghosa DOI: 10.33962/roneuro-2020-016 Romanian Neurosurgery (2020) XXXIV (1): pp. 116-122 DOI: 10.33962/roneuro-2020-016 www.journals.lapub.co.uk/index.php/roneurosurgery Microbiota Gut-Brain Axis and Neurodegenerative Disease. A systematic review on Alzheimer’s disease, Amyotrophic lateral sclerosis and Parkinson Disease Poluyi Edward Oluwatobi1, Imaguezegie Grace Keywords 2 3 Ese , Poluyi Abigail Oluwatumininu , Morgan gut dysbiosis, Eghosa4 central nervous system, gastrointestinal tract, enteric nervous system, 1 Department of Life Science, Clinical Neuroscience, University of neuroimmune system, Roehampton, London, UNITED KINGDOM neuroendocrine system, 2 Lagos University Teaching Hospital, Idi-araba, Surulere, Lagos, autonomic nervous system NIGERIA (ANS) 3 College of Medicine, University of Lagos, NIGERIA 4 Ambrose Alli University, Ekpoma, Edo, NIGERIA Corresponding author: ABSTRACT Poluyi Edward This review highlights the microbiota gut-brain axis and neurodegenerative diseases excluding studies on animal models. Gut microbiota is capable of modulating some Department of Life Science, Clinical brain activities via the microbiota gut-brain axis. A bidirectional communication exists Neuroscience, University of Roehampton, London, between the gastrointestinal (GI) tract and the central nervous system (CNS) in the United Kingdom microbiota gut-brain axis. Gut dysbiosis has been linked to neurodegenerative diseases as a result of the imbalance in the composition of its microbiota, which has [email protected] a damaging effect on the host’s health. The association between the role and mechanism of CNS disease and gut microbial is yet to be fully explored.