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Antibody Mediated Neutralization Cytolytic/Cytotoxic Immune Complex Anaphylactic

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Antibody Mediated Neutralization Cytolytic/Cytotoxic Immune Complex Anaphylactic OUTLINE Introduction Antibody Mediated Neutralization Cytolytic/Cytotoxic Immune Complex Anaphylactic Cell Mediated T-cell Cytotoxic (Killer T-cells) Delayed Hypersensitivity Antibody or Cell Mediated Granulomatous Reactions IMMUNE EFFECTOR MECHANISMS LEVELS OF REACTIONS OF ANTIGEN WITH ANTIBODY OR CELLS PRIMARY SECONDARY TERTIARY REACTION REACTION REACTION in vitro in vivo ANTIBODY MEDIATED INACTIVATION NEUTRALIZATION AGGLUTINATION, LYSIS CYTOLYTIC REACTIONS OPSONIZATION Ag+Ab AgAb IMMUNE COMPLEX PRECIPITATION REACTIONS MAST CELL ANAPHYLACTIC DEGRANULATION REACTIONS CELL MEDIATED DELAYED T-DTH HYPERSENSITIVITY LYMPHOKINES REACTIONS +Ag-> MACROPHAGE ACTIVATION BLAST CELL TRANSFORMATION T-CTL TARGET-CELL LYSIS DESTRUCTION Ab or + INSOLUBLE ANTIGEN GRANULOMA NEUTRALIZATION/INACTIVATION REACTIONS PROTECTIVE REACTIONS TOXIN NEUTRALIZATION DIPHTHERIA,, TETANUS, ANTHRAX, CHOLERA RECEPTOR BLOCKADE PERTUSSIS VIRUSES MEASLES. FLU, POLIO, HEPATITIS, PAPILLOMA, ETC. PASSIVE ANTIBODY TREATMENT – CHOLERA, EBOLA VIRUS DESTRUCTIVE REACTIONS DIABETES, HEMOPHILIA, APLASTIC ANEMIA, MYASTHENIA GRAVIS, GRAVE’S DISEASE, BULLOUS SKIN DISEASES EVIDENCE FOR NEUTRILIZING ANTIBODIES DICK AND SCHICK TESTS PEOPLE WHO RECOVER FROM STREPTOCOCCAL OR DIPHTHERIA INFECTION HAVE NO REACTION TO SKIN INJECTION OF TOXIN DUE TO PRODUCTION OF NEUTRALIZING ANTIBODY SCARLET FEVER GROUP A STREPTOCOCCUS TOXIN Sequella: Glomerulonephritis; Rheumatic heart disease (IMMUNE COMPLEX REACTION) VACCINE UNDER DEVELOPMENT TREATED WITH ANTIBOTICS PENICILLIN OR AMOXICILLIN Dale JB, et al, Current approaches to Group A streptoccal Vaccine development. In Streptoccus pyogenes ED. Ferretti, Steverns, Fichetti. U. Oklahoma Press, 2016. DICK TEST FOR SUSCEPTIBILITY TO SCARLET FEVER 1924 GEORGE AND GLADYS DICK INJECTION OF 0.1 CC OF SCARLET FEVER TOXIN INTO THE SKIN: INFLAMMATORY REACTION OF 10MM WITHIN 24 HOURS INDICATES LACK OF IMMUNITY. STAPH STREP TOXIN NO REACTION -- INDICATES IMMUNITY ANTIBODY NEUTRALIZES TOXIN Schick Test Diphtheria Toxin Bela Schick New York 1925 0.1 ml of diphtheria toxin injected into skin of one arm 0.1 ml of heat inactivated toxin into the other Individuals with toxin neutralizing antibodies will have no reaction at either site; Those without will have reaction at toxin site, but not inactivated site. VACCINES INACTIVATION / NEUTRALIZATION TOXIN NEUTRALIZATION BACTERIA TOXINS TETANUS DIPHTHERIA PERTUSSIS CHOLERA ANTHRAX RECEPTOR BLOCKADE VIRUSES MEASLES FLU EBOLA HEPATITIS HERPES POLIO PAPILLOMA ETC. DPT DIPHTHERIA - LARYNGEAL MEMBRANE PNEUMONIA TOXIN – Enters cell through receptors (EGF) and blocks protein synthesis VACCINE – HEAT INACTIVATED TOXIN PERTUSSIS WHOOPING COUGH - TOXIN AND RECEPTOR PERTUSSIS VACCINE Acellular pertussis antigens [10 µg detoxified pertussis toxin (PT), 5 µg filamentous hemagglutinin (FHA), 3 µg pertactin, and 5 µg fimbriae types 2 and 3 (FIM)]. TETANUS LOCKJAW NEONATALTETANUS OPISTHOTONOS OPISTHO – BACKWARD; TONO - TENSION PROPHYLACTIC IMMUNIZATION USING TETANUS TOXOID BACTERIA LIVE IN DEAD TISSUE TOXIN BLOCKS INHIBITORY NEURONS WHICH MODULATE ACTIVITY OF STIMULATORY NEURONS AND PREVENT THE CONTINUOUS MUSCLE CONTRACTION OF TETANUS ANTIBODY TO TETANUS TOXIN PREVENTS UPTAKE FROM DEAD TISSUES TO LIVING NEURONS CHOLERA JOHN SNOW LONDON 1854 FIRST APPLICATION OF PUBLIC HEALTH TO PREVENT DISEASE GIVEN ORALLY RECEPTOR AND TOXIN STIMULATES IgA ANTIBODY ANTHRAX VACCINE 1881 LOUIS PASTEUR Mab TREATMENT VACCINATE COWS “HERD IMMUNITY” PREVENTS HUMAN INFECTION ANTIBODY BLOCKS AT MULTIPLE STAGES OF PROCESS BINDING OF TOXIN TO RECEPTOR ASSEMBLY OF TOXIN COMPONENTS PORE FORMATION ENDOCYTOSIS TOXIN TRANSLOCATION Froude JS, Thullier P, Pelat T. Antibodies against anthrax: mechanism of action and clinical applications. Toxins 3:1433-1452, 2011 HUANIZED MONOCLONAL ANTIBODY VIRUS VACCINATION PREVENTION MOSTLY BY RECEPTOR BLOCKADE* Measles Rabies Mumps Hepatitis Rubella Chaga disease Varicella Yellow Fever Influenza Japanese Encephalitis Coronavirus Dengue Polio West Nile Zika HIV Rotavirus Ebola Etc. * ALSO T-CELL CYTOXICITY TO BE PRESENTED LATER Virus Receptor Blockade MMRV VACCINE MEASLES, MUMPS, RUBELLA, VARICELLA ATTENUATED LIVE VIRUS VARICELLA TARGET MUCOSA OF RESPIRATORY TRACT MEASLES, MUMPS , REBULLA VIRUS INFECTS MUCOSA Vaccine induced IgA antibody blocks protein receptor IgAantibody However, with direct contact with skin some skin infections ( ie. Smallpox) are not blocked by antibody and require T-CTL (more later) DISEASE RETURNS WHEN FAMLIES REFUSE VACINE POLIO VACCINES POLIO BOTH IgG and IgA ANTIBODY INCLUDES INFLUENZA, CORONAVIRUS PATHOGENESIS OF ACUTE INFLUENZA PNEUMONIA H&E-stained section of the lung from a 1918 influenza victim showing necrotizing bronchiolitis. There is necrosis of the bronchiolar wall, with submucosal edema and vascular congestion. The epithelial layer is desquamating, and necrotic epithelial cells are present in the lumen. A mixed inflammatory cell infiltrate is present throughout (original magnification400×). Taubenberger JK, Morens DM. The pathology of influenza virus infections. Annu. Rev. Pathol. Mech. Dis. 3:499-522, 2008. INFLUENZA VACCINES THREE LEVELS OF PROTECTIVE IMMUNITY 1. ANTI-VIRUS 2. ANTI-CELL MEMBRANE 3. T-CTL T-CTL TO BE PRESENTED IN DETAIL IN NEXT LECTURE INFLUENZA VACCINE Why is a “new” vaccine required every year? Antigenic drift Mutation produces “new” surface HA (hemaglutinin) INFLUENZA VACCINE KILLED OR WEAKENED VIRUS HEMAGGLUTININ ANTIGENIC COMPONENTS OF HEMGGLUTININ CHANGE EVERY FLU SEASON, NEW VARIENTS ARE SELECTED FOR EACH YEAR, •egg-based flu vaccine, •cell-based flu vaccine, and •recombinant flu vaccine. Most common Egg-based vaccine manufacturing is used to make both inactivated (killed) vaccine (usually called the “flu shot”) and live attenuated (weakened) vaccine (usually called the “nasal spray” flu vaccine MUTIPLE IMMUNE MECHANISMS IN RESPONSE TO FLU VIRUS IgA BLOCKING AB IgG NEUTRALIZING AB CYTOTOXIC T-CELLS DTH T-CELL More later SARS CoV-2 POTENTIAL IMMUNOGENS CORNAVIRUS VACCINE MODERNA ASTRZENKA mRNA-1273 Spike protein DA approved for Phase 3 clinical trials HUMAN PAPPILOMA VIRUS AND HUMAN PAPILLOMA VIRUS ANTIBODY AND T-CTL HIV NO VACCINE - INFECTS CD 4 HELPER T-CELLS AZT AZIDOTHYMIDINE THYMIDINE ANALOG BLOCKS REVERSE TRANSCRIPTASE VACCINATION PREVENTION BY RECEPTOR BLOCKADE H. Influenza HIV Meningococcus Rabies Pneumococcus Hepatitis Viral Exanthems Polio Smallpox Chagas disease Measles Yellow Fever Rubella Japanese Encephalitis Varicella Dengue Influenza West Nile Mumps Zika Ebola Typhoid Rotavirus MONOCLONAL ANTIBODIES TREATMENT WITH INACTIVATING ANTIBODIES PASSIVE TRANSFER OF MONOCLONAL ANTIBODIES FOR ANTHRAX EBOLA SNAKE VENOM EBOLA VIRUS Rial P, Elias SC. et al. (28 Co-authors) Alan R. Townsend. Therapeutic monoclonal antibodies for Ebola virus infection derived from vaccinated humans. Cell Reports 27:172-`86, 2019 NY times August 13, 2019 2018/19 Epidemic %died Untreated 70 Anti-viral 33 (Giliad) Z-Mapp 24 (Mapp Biopharm. REGN-EB3 6 (Regeneron) mAb-114 (Ridgeback Biother.) 11 ANTI-VENOM TREATMENT Kills 100,000 annually and permanently disfigures >300,000 • May 16, 2019 AVI (International AIDS Vaccine Initative)and the Liverpool School of Tropical Medicine (LSTM) have formed a research consortium to apply antibody discovery technologies to develop affordable, accessible, and effective monoclonal antibodies (mAbs) for snakebite treatment. The consortium, the Scientific Research Partnership for Neglected Tropical Snakebite (SRPNTS), also includes • The Nigeria Snakebite Research & Intervention Centre (Bayero University, Kano), • The Kenya Snakebite Research & Intervention Centre (Institute of Primate Research, Nairobi), • The Indian Institute of Science (Bangalore), • The Scripps Research (La Jolla). • The consortium is funded with UK aid from the UK government through the Department for International Development (DFID). NEUTRALIZATION DISEASES ANTIBODIES BLOCK NORMAL BIOLOGICALLY ACTIVE MOLECULES OR RECEPTORS DIABETES INSULIN, INSULIN RECEPTOR ISLET CELLS HEMOPHILIA BLOOD CLOTTING FACTORS PERNICIOUS ANEMIA PARIETAL CELLS APLASTIC ANEMIA ERYTHROID TANSCRIPTION FACTOR MYASTHENIA GRAVIS ACTEYLCHOLINE RECEPTOR GRAVE’S DISEASE HYPERTHYROIDISM THYROID HORMONE RECEPTOR LATS BULLOUS SKIN DISEASES EPIDERMAL CELLS/BASEMENT MEMB. IMMUNE FACTORS IN DIABETES . NORMAL ISLET LYMPHOCYTIC INFILTRATE HYLINIZED ISLET IMMUNOLABELING TISSUE TEST FOR ISLET CELL AUTOANTIBODIES 1. MICROSCOPIC SLIDE OF PANCREAS 2. ADD PATIENT’S SERUM, INCUBATE AND WASH 3. ADD PEROXIDASE LABELED ANTI-HUMAN IgG ROLE OF ANTI-ISLET CELL ANTIBODIES NOT CLEAR INFILTRATING LYMPHOCYTES ARE CD 8 (AUTO-REACTIVE CYTOTOXIC T-CELLS) La Torre D, Lenmark A. Immunology of beta-cell destruction. Adv. Exp. Med. Biold2010:654:537-583 doi: 10.1007/978-90-481-3271-3_24. Veld, PI. Insulinitis inhuman type 1 diabetes. Islets 3:131-138, 2011 soi: 10.4616/isl.3.4.15728 INSULIN ANTIBODIES INSULIN- NOBLE PRIZE FOR DISCOVERY – 1923 Frederick Banting and John Macleod ANTIBODIES TO EXOGENOUS ADMINISTERED INSULIN ARE COMMON WITH TREATMENT USUALLY IgG – SEVERE INSULIN RESISTENCE (AUTOIMMUNE HYPOGLYCEMIA) ALSO IgE – INSULIN ALLERGY HIGHER FREQUENCY WITH BEEF OR PORK INSULIN, MUCH LESS WITH RECOMBINANT HUMAN INSULIN MEASURED BY RIA (NOBLE PRIZE IN 1977; Rosalyn Yalow) TREATMENT – SWITCH INSULIN SOURCES GLUCOCORTICOIDS PERNICIOUS ANEMIA – Megaloblastic Anemia Failure to absorb Vitamin B12 (poor diet, gastrectomy, H. pylori infection, congenital deficiency of intrinsic factor) Immune Atrophic gastritis Auto antibodies to parietal cells NORMAL
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