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MCMP 422 Exam One Questions With Correct Answers, Exams of Advanced Education

MCMP 422 Exam One Questions With Correct Answers

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2024/2025

Available from 05/15/2025

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MCMP 422 Exam One Questions With Correct Answers
Immunology the science of how the body responds to foreign agents
Vaccinia Virus causes cowpox
Vaccination the deliberate induction of protective immunity to a pathogen by the
administration of killed or non-pathogenic forms of the pathogen, or its antigens, to
induce an immune response
How was vaccinia transmitted? from cows to humans
Edward Jenner Discovered the small pox vaccine.
How did Edward Jenner discover the smallpox vaccine? - Answer noticed milk
maids/farmers did not get smallpox, inoculated his son
Endemic - Answer consistently present or characteristic of a region
What is an example of an endemic disease? - Answer malaria to Africa and southern
Asia
Commensal Flora - Answer aggregate microbial population that inhabits a person
Probiotics - Answer microbes that have a substantiated therapeutic use
How can commensal bacteria become bad? - Answer become immunocompromised and
bacteria release toxins to damage mucus, red and white cells leak into gut between
injured cells
Opportunistic Pathogens - Answer microorganisms that causes disease in individuals
whose immune systems are compromised
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MCMP 422 Exam One Questions With Correct Answers

Immunology the science of how the body responds to foreign agents Vaccinia Virus causes cowpox Vaccination the deliberate induction of protective immunity to a pathogen by theadministration of killed or non-pathogenic forms of the pathogen, or its antigens, to induce an immune response How was vaccinia transmitted? from cows to humans Edward Jenner Discovered the small pox vaccine. How did Edward Jenner discover the smallpox vaccine? - Answer noticed milkmaids/farmers did not get smallpox, inoculated his son Endemic - Answer consistently present or characteristic of a region What is an example of an endemic disease? - Answer malaria to Africa and southernAsia Commensal Flora - Answer aggregate microbial population that inhabits a person Probiotics - Answer microbes that have a substantiated therapeutic use How can commensal bacteria become bad? - Answer become immunocompromised andbacteria release toxins to damage mucus, red and white cells leak into gut between injured cells Opportunistic Pathogens - Answer microorganisms that causes disease in individualswhose immune systems are compromised

Pneumocystis Carinii - Answer problem in AIDS patients Why is psuedomonas a problem in cystic fibrosis patients? - Answer they acquireexcess mucus in the lungs they cannot clear, bacteria thrives in moist environments and colonizes What are the four major classes of pathogen? - Answer bacteria, fungi, viruses,parasites

What are helminths? - Answer parasitic worms What are the barrier types? - Answer mechanical/physical, chemical, microbiological What are the mucosal tracts? - Answer respiratory, urogenital, gastrointestinal Lungs - Answer mucus, cilia trap and move pathogens, expulsion by swallowing orsneezing

Nose - Answer mucus traps pathogens which are then swallowed or blown out Mouth - Answer commensal microbes, saliva Eyes - Answer lysozyme produced by lacrimal glands Stomach - Answer acid neutralization, pH of 1- Intestine - Answer commensal microbes, mucus protects cells from digestive enzymes Urogenital Tract - Answer slightly acidic conditions, lactic acid from lactobacilli

pathogens Endocytosis - Process by which material from the outside of cell is taken in Lectins - Carbohydrate molecules which bind to carbohydrates on pathogen How does the innate immune response cause inflammation at sites of infection? -Bacteria causes cleavage of complement protein. Complement protein covalently bonds to bacteria. The other piece of the complement attracts effector cell. Complementreceptor on effector cell recognizes the complement fragment on bacteria. Effector engulfs bacteria How do the effector cells promote inflammation? -Answer microbes from wound come incontact with effector cell, effector cell secretes cytokines, vasodilation and increased vascular permeability allow inflammatory molecules into tissue Cytokines -Answer signaling molecules of innate and adaptive immunity, induceinflammation and other immune responses

Selectins -Answer adhesive molecules on leukocytes and endothelial cells Where do the selectins occur? -Answer white blood cells surface What happens when inflammation is elicited? - Answer dilation of the blood capillaries(heat and redness) vascular dilation (swelling and pain), extravasation

Extravasation - Answer movement of cells/fluid into connective tissue, changesadhesiveness of endothelial tissue allowing attachment and migration of immune cells, vascular dilation, movement from blood to infection site Characteristics of Innate Immunity - Answer rapid response, fixed, limited number of

specificities, constant during response Characteristics of Adaptive Immunity Since the response is slow, variable, highlyselective for specificities, and it improves during a response.

Leukocytes Those white blood cells that increase the immune response towards anongoing infection.

Clonal Expansion It works to find the best match for the pathogen and produces more ofthose cells.

Immunological Memory Pathogen recognizing lymphocyte may persist to respond fasterwith next exposure

What is the effect of no innate immunity? -Answer no competition for microorganisms Hematopoiesis -Answer to make immune system and blood cells Pluripotent Stem Cells -Answer hematopietic stem cell, can become many other types ofcells, can make copies of themselves, regenerate themselves

What is the common lymphoid precursor product? -Answer B cell, NK/T cell precursor What is produced by the common myeloid precursor cell? - Answergranulocyte-macrophage progenitor, megakaryocyte/erythroid progenitor

B cell -> ________- Answer plasma cell T cell -> ________- Answer effector T cell

Monocyte -Answer circulate in blood immature form of macrophage Macrophage -Answer scavengers phagocytose pathogens cells debris secretecytokines

What cells are lymphoids? -Answer B cells T cells NK cells What cells are myeloids? -Answer dendritic cells mast cells monocytes macrophages What cells are granulocytes? -Answer neutrophils eosinophils basophils Neutrophils -Answer most abundant phagocyte effector cells of innate immunityshort-lived dead form is pus

Eosinophils-Answer target worms and intestinal parasites, amplify inflammation, bindIgE, very toxic to pathogen and host, lead to chronic asthma

Basophils -Answer rare, unknown function What cells are erythroids? -Answer megakaryocyte, erythrocyte Megakaryocyte -Answer giant nucleus, resident of bone marrow, fusion of precursorcells, fragments make platelets

Erythrocytes -Answer red blood cells, gas transport, used by pathogens to evadeimmune detection

What are erythrocytes infected by? - Answer plasmodium falciparum (malaria)

What is the sequence of hematopoietic production? - Answer yolk sac, fetal liver andspleen, bone marrow

How does hematopoietic cell production go as you age? - Answer decreases What is the breakdown of a CBC? - Answer 40-75% neutrophil, 1-6% eosinophil, <1%basophil, 2-10% monocyte, 20-50% lymphocyte

What is the pathway of neutrophils? -Answer stored in bone marrow, released wheninfection is present, travel and invade infected tissue, engulf and kill bacteria, die in tissue and engulfed and degraded by macrophages Antibody Neutralization -Answer bind toxins so they cannot be taken into the cell tocause damage

Antibody Opsonization -Answer make large complexes to be phagocytized Where do most lymphocytes reside? Ans: Peyer's patch, thoracic duct, lymphatics,thymus, bone marrow, spleen

Primary lymphoid tissues- Which of the following are primary lymphoid tissues? Ans:thymus and bone marrow

Red Bone Marrow In what organ does production of WBCs take place? Thymus development of which cells takes place here? Thoracic Duct name the main lymphoid pathway Lymphatic Vessels name the lymphatic fluid collection

White Pulp - Answer immune system tissue, cells enter and leave by blood How is the spleen organized? -Answer white pulp is within red pulp How is the white pulp organized? -Answer central arteriole, perifollicular zone, marginalzone, germinal center, B cell area, lymphoid sheath

What would be reason for splenectomy? -Answer autoimmune disease, injurymalignancy

Cogenital Asplenia -Answer hereditary immunodeficiency, born w/out spleen, microbialinfections

M Cells - microfold cells, capture pathogens from gut lumen to underlying lymphoidtissue

What are the extracellular spaces pathogens can live? - interstitial spaces, epithelialsurfaces

What are the intracellular spaces a pathogen can live? - cytoplasmic, vesicular What is unique about viruses? - can live intracellular and extracellular, requires hostmachinery to survive

Where are complement proteins synthesized? - liver Zymogen - The inactive form of an enzyme Which, A or B is smaller? a

What about I in complement? Inhibitory Protease Amplification Cascade The stimulus causes the activation of the zymogen 1 toprotease 1; protease 1 activates zymogen 2 to protease 2

Protease Signal Transduction Cascade - Answer epinephrine binds to G-protein linkedreceptor, activates G protein, which activates adenylyl cyclase, which converts ATP to cyclic AMP, which activates protein kinase A which in turn activates phosphorylasekinase, which activates glycogen phosphorylase, which then converts glycogen into glucose-1-phosphate How does complement bind to a pathogen? - Answer thioester bond and nucleophilicattack to form covalent bond

Steps of Complement Fixation - Answer C3 cleaved into C3a and C3b, C3a recruits otherimmune cells, C3b attaches to bacteria or hydrolyzed by water

What is present on a pathogen for the attachment of C3b? - Answer hydroxyl or aminegroup

List the complement pathways in order. - Answer alternative, lectin, and classical Alternative Pathway Steps-Answer pathogen surface creates environment forcomplement activation, first to act, cleavage of C3, recruits inflammatory cells

Steps of Lectin Pathway-Answer mannose-binding lectin binds to pathogen, second toact, cleavage of C3, opsonization of pathogens

Steps of Classical Pathway-Answer C reactive protein binds to specific antigen onpathogen surface, third to act, cleavage of C3, perforation of pathogen cell membrane

What would happen if a patient is Factor I deficient? - Answer C3 convertase C3bBb isunchecked, C3 depleted, fix small amounts of C3b on cell surfaces, less clearing of phagocytes What are the mechanisms of bacterial mimicry? - Answer factor H attached to humancells via sialic acid to reduce activity of C3b, choline phosphate attaches to bacterial surface for adhesion to eukaryotic platelet-activating factor receptor Steps of Phagocytosis - Answer CR1 on macrophage binds to C3b on pathogen,endocytosis of bacteria, macrophage membranes fuse making phagosome, lysosomes fuse to make phagolysosome Can phagocytosis occur without complement activation? - Answer yes, just less efficient Formation of Membrane Attack Complex - Answer C3b binds to alternative C3convertase, alternative C5 convertase is formed, C3b2Bb, C5b initiates membrane attack complex C5 - Answer C5b fragment initiates assembly of membrane-attack complex C6 - binds and stabilizes C5b, forms binding site for C C7- binds to C5b6 and exposes hydrophobic region for attachment to cell membrane C8- binds to C5b67 and exposes hydrophobic region that inserts into cell membrane C9- polymerization on C5b678 complex to form membrane-spanning channel thatbreaches the integrity of the cell and can lead to its death.

Anaphylatoxins - Answer elicit inflammatory response

What is the action of C3a and C5a? - Answer increase vascular permeability to accessbacteria and immune cells recruitment

Coagulation System - Answer plasma enzymes form clotting blood, platelet releaseproteins for wound repair and microbial defense, pathogens release proteases to aid invasion What causes septic shock? - Answer entry of pathogens into blood stream Alpha 2-Macroglobulin - Answer inactivate bacterial proteases How does alpha 2-macroglobulin work? -Answer protease cleaves bait region forconformational change, alpha 2 covalently bonds to protease

Why are amphipathic proteins important in killing pathogens? -Answer havehydrophobic and hydrophilic region to perforate membrane

What cells secrete alpha-defensins? -Answer neutrophils and paneth cells What cells secrete beta-defensins? -Answer epithelial cells What form do alpha and beta-defensins usually come in? -Answer inactive in blood,require specific conditions to become active

Pentraxins -Answer composed of five various subunits, innate counterpart of antibodies,stimulate phagocytosis, vary glycocalyx for various functions and affinities

How is it that pentraxins works? -Answer by binding to the surface of the pathogen andphagocyte to enhance phagocytosis

IL-6 - Answer acts on muscle and fat cells to elevate temperature NOD-Like Receptors - Answer recognize bacterial breakdown products in thecytoplasm, cytosolic

What is the composition of the NOD-Like receptors? -Answer LRR domain to recognizedegradation products, nucleotide-binding oligomerization domain to initiate kinase cascade Inflammasome -Answer protein complex that increases the production of IL-1b, cleaveprocaspase to activate more inflammatory cytokines

How does the inflammasome work? -Answer self-cleavage of procaspase 1 to capsase 1to IL-1b, IL-1b production is increased by feedback loop

What are adhesion molecules of neutrophils? - Choose selectins, addressins,chemokines

Selectins - Cellular adhesion molecules that bind to sugar Addressins - Large family of proteins and ligands for lymphocytes Diapedsis - Squeezing of cell into infection site Steps of Neutrophil Recruitment - Rolling adhesion, tight binding adhesion, diapedesis,migration

Rolling Adhesion - Answer P selectin on endothelial cell binds to s-lewis antigen onWBC, slows down so neutrophil can squeeze through

Tight Binding - Answer LFA-1 on WBC binds to ICAM-1 on endothelial cell to stop WBC How do chemokines signal other cells? - Answer bind to receptor, recruits G protein,changes gene expression

How do neutrophils destroy pathogens? - Answer respiratory burst, hypochlorous acid,hydrogen peroxide, catalase

Respiratory Burst - Answer increase pH of phagosome to activate antimicrobial proteinslike NADPH oxidase and superoxide dismutase

What is the function of NADPH oxidase? - Answer catalyzes NADPH and oxygen intoNADPH and superoxide

What is the function of superoxide dismutase? - Answer catalyzes hydrogen andsuperoxide into hydrogen peroxide and oxygen

What is the function of catalase? - Answer catalyzes hydrogen peroxide into water andoxygen

What does myeloperoxidase do? -Answer catalyzes hydrogen peroxide and chloride intohypochlorous acid and water

What happens after neutrophils die? -Answer form a net to trap pathogens Chronic Granulomatous Disease -Answer CGD, more susceptible to disease, form largergranulomas, no respiratory burst or increase in pH, pathogens aren't cleared, make chronic pathogen What are some advantages of fever? - Pathogen doesn't replicate as quickly, adaptiveimmunity stronger

What is the pathway that mannose-binding lectin takes? -Answer MBL binds pathogen,MASP-2 self-cleaves, C4b covalently binds to microbe, MASP-2 cleaves C2, C2a binds surface C4b forming classical C3 convertase C4bC2a, cleaves C3, C3b binds microbe What are the steps of C-reactive protein classical activation? -Answer CRP bindsphosphocholine on pathogen, C1 binds CRP to initiate classical pathway, C1 cleaves C and C2 making C4bC2a, convergence of classical and lectin pathways What are the two types of toll-like receptors? -Answer plasma membrane andintracellular group

What does TLR4 bind to? -Answer LPS Where is the intracellular TLR found? -Answer on endosomes What does TLR3 bind to? - Answer dsRNA Are cell-surface or endosomal TLR more variable? - Answer cell-surface Type 1 Interferon - Answer inhibits viral replication in infected and surrounding cells,alert lymphocytes to kill infected cell

How does Interferon 1 respond to a virus? - Answer changes gene expression on a largescale

What is unique about interferons? - Answer they can be autocrine and paracrine What do IFN-alpha and IFN-beta do? - Anwer Induce resistance to viral replication in allcells, increase expression for receptors on NK cells, activate NK cells to kill virally-infected cells

Plasmacytoid Dendritic Cells - Anwer Like plasma cell, best at producing type 1interferon

What does the initial infection cause? - Anwer burst in releasing cytokines What is the mechanism behind interferon activation of NK cells? -Answer infectioninduces a burst in cytokine production, enhances proliferation and activation of NK cells, NK cells contain viral replication and prevent pathogenesis until Tc cells becomeavailable.

What are the two subpopulations of NK cells? -Answer CD56 dim and CD56 bright CD56 Dim -Answer low levels of expression of CD56, highly cytotoxic CD56 Bright -Response uterine NK cells, low cytotoxicity, development of blood vesselsfor the placenta

What are the two major pathways of NK cell signaling? -Response TLR7 and TLR TLR7 Pathway -Response TLR7 recognizes ssRNA, MyD88 becomes phosphorylatedand activates IRF7, this results in the production of IFN-α and IFN-β

TLR3 Pathway -Response TLR3 recognizes dsRNA, TRIF mediates the activation ofserine-threonine kinases, which activates IRF3, only IFN-β is produced

How do macrophage activate NK cells? -Answer macrophage produce IL-12, NK cellsbecome effector NK cells

How is the balance between NK cells and dendritic cells? -Answer more NK cells, onlyinnate immunity; fewer NK cells, transition into adaptive immune response