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Unit 3 Study Guide

by: Kayla Robinson

Unit 3 Study Guide BIOL 4201

Kayla Robinson
GPA 3.92

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About this Document

Here is my study guide for the next exam! Good luck! (The study guide is created before Dr. Goven gives out his personal study guide sheet)
Dr. Goven
Study Guide
immunology, exam
50 ?




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This 6 page Study Guide was uploaded by Kayla Robinson on Sunday April 10, 2016. The Study Guide belongs to BIOL 4201 at University of North Texas taught by Dr. Goven in Winter 2016. Since its upload, it has received 110 views. For similar materials see Immunology in Biology at University of North Texas.


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Date Created: 04/10/16
Unit 3 Study Guide from Notes T-delayed type hypersensitivity cells  Ex. TB skin test o Use purified protein derivative (PPD) of Mycobacterium tuberculosis o If you have tuberculosis, skin test will be positive  Sensitization phase (tuberculosis Ag introduced into the body) o Ag meets with the Antigen Presenting Cell (in regional lymph node) o APC now forms a Class 2 bridge with a T helper cell o Proliferation of H and TDTH  Effector Phase (tuberculosis-sensitive T cells go after the Ag) o TDTHbinds to the PPD o Produce cytokines—chemotactic and arming o Attract macrophages  Form granulomas (giant cell cyst-like blockage of the bacteria)  Can kill some PPD, but mostly wall off Theory: T DTHrelease Macrophage Inhibitory Factor (MIF) to stop macrophages from migrating in certain situations  Proof: Mouse injected with Egg Albumin (EA) and nutrient broth as an irritant —macrophages will be attracted  Collect wbc and centrifuge to collect macrophages in capillary pipette  Two plates: Experimental—Add EA; Control—NO EA  Experimental plate shows minimal migration of macrophages from the pipette to the EA  Proof that TDTHcells produce MIF o T cells here were produced by the original infection with EA DTH Tumor cells produce Tumor Associated Antigens (TAA)  When TAA are shed from an endogenous tumor, become exogenous antigens  Activate macrophage, Class 2 bridge, T ,Hand T CTL TCTL  Will only multiply IF: bind Ag and activated by IL-2 from T cells H  Can kill the cell  Causes vacuole with perforin proteins to fuse to the target cell membrane  Perforins form a tube (just like with complement) that will cause cell to lose integrity  Granzymes will also be released into target cell, causing death  Very efficient, can kill multiple targets quickly  Transplant can be attacked very quickly TCTLExperiment o Add macrophages, T cells, B cells—100% of a tumor cell killed o Add CD8—30% killed o Add CD4—5% killed o Add CD8 and CD4—90% killed Results: 1. macrophages not as important in tumors (endogenous) Why? Because endogenous Ag are smaller, do not need to be processed by macrophages 2. Need CD4 AND CD8 cells (T aHd T CTL 51 Cr Release Asssay o Purpose: How to measure number of target cells lysed o Use xenogeneic (other species) Ag in a mouse-- goat cells o Tissue culture with nutrient labeled with51Cr o Goat cells have 5Cr in them now 51 o Add T cells, observe amount of Cr in fluid (that was released by the lysed goat cells) o Compared against a standard curve Abnormal Immune Function Four Types of Hypersensitivity (allergy) Type I: Immediate  IgE mediated  Binds to IgEFc receptor on mast cell in tissue  Causes mast cell degranulation with reexposure  Reaction in gut—diarrhea; lungs—rhinitis; skin—hives 1. Sensitization phase: during early exposure, forms memory cells  More exposure leads to more sensitization and memory cells 2. Elicitation phase: make enough IgE to show signs and symptoms a. IgE begins to fill receptors on mast cell b. Reexposure: Ag binds to IgE on the mast cells c. Degranulation of mast cells: Release vasoactive amines, cause leaky vasculature d. Release of histamine (pre-formed), prostaglandin, and leukotrienes (long term) 3. Treatment a. Prevention: remove allergen, modify behavior b. Drugs: antihistamines (competitive inhibitor), steroids (immunosuppressant), broncodilators (relax smooth muscle, better air movement) c. Immune Desensitization: allergy shot – low doses of inhaled allergens i. Injected intramuscular ii. Want to change type of Ig made from E to G iii. Need regular shots to keep IgG levels high enough d. Acute Desensitization: used when allergic to a needed drug i. Give small dose- will show mild symptoms ii. Give more small doses every half hour iii. Degranulate all mast cells periodically instead of all at once iv. Give therapeutic dose when all mast cells have been degranulated Type II: Cytotoxic  IgM and IgG  Can be caused by autoantigen or exogenous  Can take 5-6 days  Red urine: some drug precipitates on rbc, rbc are lysed, pigment filtered out by kidneys (ex. Penicillin for gonorrhea) 1. Ag associates with membrane of target cell 2. Ab associates with Ag 3. Complement associate—cell is lysed Type III: Immune Complex  IgM and IgG  Immune complexes small, soluble  Ab-Ag complex binds to membrane  Complement binds—cell is lysed  C3 and C5 draw in neutrophils, enhance inflammation  Serum sickness: inflammatory rxn destroys kidneys Type IV: Delayed Hypersensitivity Has been discussed at length Types of common irritants: Poison ivy: by the time T cells are ready, allergen is usually DTH washed away Deodorant: continuously on skin Perfume: if used only rarely, sensitization happens slowly Tumor Immunology Terms Hyperplasia—uncontrolled proliferation of cells  Lose regulatory ability to stop growth  Lose contact inhibition (normal cells stop growing when touch, tumor cells can create masses of cells) Anaplasia—structural abnormalities  Revert back to embryological conditions Invasiveness—form filamentous extensions Metastasis—spread to distant sites  Can live in different environments, adaptable Cachexia—wasting away Most cancer patients die from infection caused by the cancer and the treatment About 20% die from the actual cancer taking over the organ Types of Cancer Carcinoma: 85%, from epithelial cells  Skin, lung, prostate, colon  Older patients  Lead to surgery  Solid tumor  Common, caused by exposure to environment Sarcoma: 2%, from connective tissue  Bone, muscle  Also contains leukemia and lymphoma o Lots of treatment and research because cells are free and easy to work with o Young people Mixed Tumor: rare, somatic and germinal cells together Central Concepts of Tumor Immunology 1. Tumor cells have tumor associated antigens 2. Immune system can recognize TAA and make an immune response Types of TAA 1. Integral membrane protein  Well anchored in membrane  “protective” TAA  If T cell binds, will form a strong bond and kill the cell 2. Peripheral membrane protein  Weakly bound  Can be shed  T cell can lose its hold easily  “blocking” antigens—can keep surrounding T CTLusy 3. Internal  Inside the cell, only visible when cell is lysed 4. Diagnostic  Measure levels to determine degree of infection 5. Neoantigen  New antigen rising from mutated cell  Recognized easily 6. Oncofetal  Embryonic  Not a good immune response to these  Not used diagnostically because of possible false positives Immune Response Against TAA Experiment: 1. Infect Mouse A with tumor under the skin 2. Ligate tumor with a rubber band until it falls off – Mouse A is cured 3. Kill Mouse A, take T/B cells that are immune to his specific TAA 4. Transfer immunity to Mouse B 5. Infect Mouse B with same tumor cells—Mouse B shows immunity 6. Infect Mouse B with different tumor cells—Mouse B gets cancer Results: Yes, there is a specific immune response to Tumor Associated Antigens Concommitant immunity: immunize someone against a cancer they already have to avoid metastasis Can immunize against private TAA: not used widely because we can’t predict which cancer you will get Immunological Surveillance  Tumor cells are arising and being eliminated all the time by T CTL  Evidence: de novo cancer in transplants o Majority of patients with cured cancer got cancer again after transplant o Transplant surgery requires immunosuppression, decrease immunological surveillance  Neuroblastoma in children: autopsy on kids from car wrecks o Showed 4x greater incidence than kids who died from it o Shows a spontaneous regression of tumor when immune system matured  Immunosuppressed people get more cancer but not the common ones How Tumor Cells Avoid Immunological Surveillance 1. Blocking TAA keeps T cells busy 2. Ab against a tumor can actually cause rapid growth  If Ag is bound to Ab, CTLcan’t bind to it 3. Tumor cells suppress MHC1 4. Tumor cells secrete a mucopolysaccharide that covers the membrane and markers in mucous Skin Testing We’ve discussed Type IV with TB, can also be shown with “scratch test” with a fork. Tests for macrophage and cytokine activity for red and swollen skin. For Type I, can inject an allergen into skin on back. “wheal and flare test.” Positive reaction if red and swollen. Winn Assay Purpose: Test what part of immune system reacts to cancer, and how it can be enhanced to fight more efficiently. Will test potential outcome of immunotherapy. Not 100% accurate because sample is not representative of the whole body. Immunodiagnosis: measure concentration of tumor cell product to give an idea of number of tumor cells Ex. Carcinoembryonic Ag in colon cancer Immunotherapy: Can elicit immune response at the site to cause the body to recognize the cancer Ex. Nonspecific inflammation by Freud’s adjuvant Ex. Add an adjuvant to elicit a response that will kill melanoma cells as well as other skin cells Ex. Ab against the TAA- use a radioisotope to locate cancer Ex. Filter out lymphocytes and add mitogen to help the cells proliferate. After two weeks, remove new lymphocytes and inject this high count lymphocyte soln into patient. Repeat mitogen addition with the just-removed lymphocytes. Repeat: try to attack as much Ag as possible with as many lymphocytes as can be produced in the two weeks.


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