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by: Beatrice Deckow I

Immunology BIOL 452

Beatrice Deckow I
GPA 3.73

Marcia Coss

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Marcia Coss
Class Notes
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This 4 page Class Notes was uploaded by Beatrice Deckow I on Monday September 28, 2015. The Class Notes belongs to BIOL 452 at George Mason University taught by Marcia Coss in Fall. Since its upload, it has received 8 views. For similar materials see /class/215106/biol-452-george-mason-university in Biology at George Mason University.


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Date Created: 09/28/15
Chapter 10 Adaptive Immunity to Infection 1 59 9 V39 gt1 9 t O O D ID ID I ALAN D ID ID ID I OONONUI ND I 00 Describe the course of a typical acute infection a 04 hours b 496 hours c 96 hours Describe the phases of the infectious process Describe the protective responses of the immune system at each phase of the infective process What are the 5 main types of pathogenic microorganisms a b c d e What are the 3 sites of infection within the body a 1 blood b 2 tissue c 3 What are the mechanisms of the immune response to pathogens found in the 3 different body compartments Tissue damage from pathogens can occur by direct as well as indirect mechanisms List and describe 3 effects each for direct and indirect tissue damage as a result of infection What are the three ways in which the epithelium is a barrier to infection Give specific examples of each way a l b 2 c 3 Why do macrophages have a central role in immunity What is extravasation Why is it important a The movement of cells or uid from win blood vessels to the surrounding tissues b Important because What is diapedesis a The movement of blood cells particularly leukocytes from the blood across blood vessel walls into tissues What is meant by Tcell trapping How is differentiation of naive CD4 Tcells affected by the cytokines released in response to pathogens What are NKl1 Tcells a How do the different Tcell subsets in uence development of each other How does the nature and concentration of Ag affect CD4 T cell differentiation What is the primary focus Where does it occur What cells are involved What are the different effector mechanisms important in clearing infections caused by viruses bacteria fungi protozoa What is the consequence of activating the adaptive immune system Immediately and long term What is protective immunity Protective immunity is the resistance to a specific pathogen that results from infection or vaccination It is due to the adaptive immune response which set up immunological memory of that pathogen What is meant by the term immunological memory Memory is the ability of the immune system to respond more rapidly and more effectively on a second encounter with an Ag It is specific for a particular Ag and is longlived What is meant by original antigenic sin What is the mechanism OAS is the tendency of humans to make Ab responses to those epitopes shared bw the first strain of a virus they encountered and subsequent related viruses while ignoring other highly immunogenic epitopes on the second and subsequent viruses 23 How do the primary and secondary immune responses differ Chapter 12 Failures 0f the Host Defense Mechanisms 1 What is the difference between antigenic drift and antigenic shift a Antigenic drift point mutations in viral genes cause small differences in the structure of the viral surface Ag s b Antigenic shift a radical change of viral surface proteins due to a reassortment of a virus s segmented genome 2 What is viral latency Why is this important a Viral latency is when a virus has entered a cell but hasn t replicated b It is important 3 List and describe 9 defense mechanisms of the immune system to protect against infection 4 List and describe the 39 39 J quot have A 39 I J to evade the defenses of the immune system you listed in question 3 5 What is the difference between a primary and a secondary immune deficiency 6 What is the number one cause of immunodeficiency in the world In developed countries a Malnutrition b Inherited immune deficiencies 7 What are the 2 different forms of leprosy How do the immune responses differ in the two types and how does that lead to the different forms of the disease a Tuberculoid b Lepromatous CMI is depressed primary Th2 response amp pathogen is not controlled 8 When was the first immunodeficiency disease identified What was it What is the cause of the disease What is the immune defect a 1952 Dr Bruton discovered Xlinked agammaglobulinemia XLA b Characterized by absence of serum Ab Recurrent bacterial infections c Defect in the Btk gene on the Xchromosome B cells stop at preB stages 9 Give examples of the 12 possible major sites of involvement of immunodeficiency disorders 10 What general patterns of infection would you see with the following deficiencies a Stem cell b Tce119 susceptible to fungi worms viruses higher cancer rates SCID c B ce119 decreased Ab levels repeated infections with pyogenic bacteria d Phagocyte e Complement 11 Stem cell deficiencies a SCID severe combined immunodeficiency b ADA adenosine deaminase deficiency c PNP purine nucleotide phosphorylase deficiency l2 Thymus hypoplasiaabnormalities DiGeorge syndrome 13 Tcell deficiencies WiskottAldrich Syndrome what is the defect a Defect in the WASP gene decreased amp function of Tcells and affects plateletls and blood clotting l4 NK defects ChediakHigashi syndrome what is the defect a CSHl defect partial albinism abnormal platelet function sever immune deficiency 15 B cell deficiencies a XLA Xlinked agammaglobulinemia Bruton39s i Defect in Btk gene Bcells stop at preB stage repeated infections without memory b Immunode ciency with hyperIgM i Patients have normal B amp T cell development with high IgM levels to TI Ag s limited IgM response to TD Ag s mutation in CD40L gene c Transient hypogammaglobulinemia of infancy i Occurs bw 612 mo s of age slow to start producing IgG d Selective IgA hypogammaglobulinemia i Most common inherited primary immunode ciency no obvi disease susceptibility treated by antibiotics l6 Phagocyte defects a LAD leukocyte adhesion de ciency i Leukocyte B2 integrin defects b CGD chronic granulomatous disease i Cells cannot produce ROS susceptible to chronic bacterial infections which can lead to formation of granulomas l7 Complement defects Heriditary neurotic angioedema a Defect with Clinhibitor leads to accumulation of uid in tissues 18 What are several causes of secondary immunode ciencies 19 What are several nonimmunological abnormalities that may lead to increased susceptibility to infection 20 AIDS 7 Acquired immune de ciency syndrome Describe the HIV viral structure amp genome characteristics 0 Envelope derived from host cell membrane has one type of peplomer Peplomers 72 identical surface glycoproteins Genome 2 identical ssRNA Capsid encloses the 2 ssRNA segments amp the 3 enzymes Enzymes RT copies RNA 9 cDNA Protease cleaves viral proteins Integrase inserts cDNA into host cell s DNA Describe the normal replication mechanisms of HIV 0 RT copies RNA into cDNA cDNA goes into host nucleus and is inserted to host DNA with help from Integrase Provirus Provirus is the transcribed by host cell RNA polymerase to make viral mRNA Viral mRNA is translated into viral polyproteins What role do the chemokine receptors play 0 CD4 CCR5 CXCR4 serve as coreceptors for HIV Discuss the cause of depletion of CD4 T cells I 0000 o Discuss the role of CD8 T cells 0 Describe the immune response during the course of HIV AIDS 0 Describe approaches to treatment 0 Describe approaches to vaccines o What does AIDS screening tell you 0 Chapter 13 Allergy and Hypersensitivity 9 8094 9 What are the four types of immunemediated hypersensitivities How do they differ How does each type mediate its tissue damage What are the effector mechanisms What is the time course for each type What is an allergen IgE allergic reactions are classi ed according to their clinical effects syndrome describe the differences between the classes What is atopy How does it relate to allergic asthma How does an allergic response occur What is desensitization and how does it work Why is this done What are the different routes of entry for allergens How does the dose and route of entry affect the response What are some common features of inhaled allergens and how do these features affect the immune response How do genetic factors contribute to an allergic response How does the cytokine environment affect the allergic response See Fig 87 What is anaphylaXis How does systemic anaphylaXis occur What is urticaria What is it a response to How are the different phases of allergic responses treated What is the wheal and are reaction What are the two different populations of mast cells How do their effects differ when triggererd What is meant by preformed mediators of mast cells How do these differ from the newly formed ediators What effect do mast cell mediators have on different tissues What about eosinophil mediators What is the difference between immediate and late phase allergic responses How do Type II and Type III hypersensitivities differ What are immune complexes Why can they become a problem What is an Arthus reaction How does it occur What cells are involved What is the time course What is serum sickness When is it seen How does it occur What it39s time course What is farmer s lung What type of hypersensitivity is it What causes the tissue damage What does DTH stand for How does it occur What is the time course What cytokines are involved in the response What are three types of Type IV hypersensitivities How do the consequences differ What is contact hypersensitivity How does this play a role in poison ivy What cytokines are involved in a DTH reaction Why doesn39t everyone suffer from allergies Chapter 14 Immune Response in the Absence of Infection 1 2 wasgwe What is autoimmunity How is it caused What is the relationship between autoimmunity and genetic and environmental factors What are the mechanisms of tissue damage What is IDDM What is the relationship between IDDM and MHC HLA genes What is the mechanism ofthis disease What is autoimmune hemolytic anemia What type of hypersensitivity is this How and when does it occur What is Goodpasture s syndrome How does it occur What is the difference between tissue organ and systemic autoimmune diseases What is Grave39s disease What is the autoantigen What is the mechanism of the disease What is myasthenia gravis What is the autoantigen What is the mechanism of the disease What is SLE What is the common autoantigen What is the mechanism of this disease How can an autoimmune disease be diagnosed Why is a Type II or III autoimmune disease easier to diagnose than a Type IV autoimmune disease


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