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immunology
exam 2
| Question | Answer |
|---|---|
| importance of the immune system | 1.recognize and eliminate pathogens 2.recognize and eliminate distressed, damaged, diseased, and dead cells. 3.discern b/w self and nonself |
| role of immune system | 1. defense against infections 2. defense against tumors 3. induce pathologic inflammation 4. recognize and respond to tissue grafts and newly introduced proteins |
| Small pox varolation | 12th century. chinese took scabs and rubbed them into cuts of children. acts as exposure and "vaccine" |
| Rinderpest inoculations | 1754.viral infection in ruminants. when given small dose of virus animals have immunity. |
| Edward Jenner | 1798. cowpox, term"vaccination" developed |
| Pasteur's fowl | 1879. fowl cholera experiment. chickens given killed virus are immune when introduced a second time with live virus. |
| What vaccines did Pasteur develop | anthrax and rabies |
| Daniel Salmon and Theobald Smith | dead organisms can make effective vaccines |
| Von Behring and Kitasato | bacteria products also protective. Tetnus toxoid |
| Commensals | colonize body surfaces but do not invade the body and don't normally cause disease |
| Pathogen | organism than can cause disease |
| Primary pathogen | cause disease every time it invades body, even in sm. # |
| oportunistic pathogen | cause disease only when administered in high doses |
| Bodies defenses | 1. biochemical and cellular rxns 2. no immune response is restricted to a single biochem mechanism/pathway 3. redundant and multiple mechanisms work together to ensure microbial destructions |
| Innate defense | 1. Protect previously unexposed animals 2.immediate protection 3. Not specific 4.PAMPS/DAMPS 5.Important signals for adaptive immune response |
| Adaptive defense | 1. Develops days to wks after exposure 2. specific 3.memory 4.knows self vs non self 5. enhances innate immune response |
| components of innate defense | 1. physical/ chem barriers 2. phagocytic and sentinel cells 3.complement system 4.innate defense cytokines 5. NK cells |
| Physical/ chemical barriers | 1. Epithelial barriers 2. normal microflora 3. acid env in stomach 4.antimicrobial peptides |
| Phagocytic cells | ingest and kill pathogens |
| Phagocytic cell ex | Neutrophils and Macrophages |
| Sentinel cells | resident tissue cells that detect invasion by recognizing PAMPs and DAMPs |
| Sentinel cell ex | DC, macrophages, mast cells |
| Complement system | An enzyme cascade system that has antimicrobial activity. Rapidly induced. Non specific. Multiple mechanisms. Potent. Harmful if not regulated |
| Cytokines | protein messenger molecules that can act on other cells or the cell that produced it. function as mediators of immune and inflammatory |
| Proinflammatory cytokines | secreted by sentinel cells in response to PAMPs and DAMPs. |
| What do proinflammatory cytokines cause | fever, lethargy, loss appetite |
| Examples of proinflammatory cytokines | IL-1, IL-6, TNF |
| Chemokine | cause cells to migrate to sites of infection, some are produced by sentinel cells. stimulate leukocyte movement. regulate migration of leukocytes from blood to tissues |
| Interferons | interferes with replication of some viruses, produced by virally infected cells |
| NK cells | lymphocyte that is part of innate immunity. kill virus infected cells and tumor cells. recognize and kill cells that do not express normal proteins |
| What are the overarching 2 components of the adaptive defense | 1. Humoral immunity 2. cell mediated immunity |
| Humoral immunity is composed of what component | antibodies |
| Cell mediated immunity is composed of what components | T helper cells, cytotoxic T cells, Gamma Delta T cells |
| Humoral immunity | transfer of body "humors" from protected animal to naive animal could provide protection |
| Cell mediated immunity | Transfer of cells from protected animal to naive animal could provide protection |
| Alpha beta T cell examples | T helper cells and cytotoxic T cells |
| Gamma delta T cells examples | Lymphocytes found in gut mucosa |
| Antigen recognition | APCs, different from recognition by innate cells |
| APCs examples | DCs, macrophages, B cells |
| When does hematopoiesis begin | with pluripotent stem cell. express CD34. self renewing |
| What cell lineages arise from hematopoietic stem cells | 1. Erythroid progenitor cell 2. myeloid progenitor cell 3. lymphoid progenitor |
| Erythroid progenitor cell examples | Erythrocyte, megakaryocyte (thrombocyte) |
| Myeloid progenitor cell examples | Myeloid cells: eosinophils, basophils, neutrophils, monocytes |
| Lymphoid progenitor cell examples | lymphocyte and NK cells |
| Leukocyte | any WBC. destroy microbes, clear damaged cells and promote more inflammation and repair |
| Mononuclear cells | lymphocyte or monocyte |
| Lymphocyte | type of WBC. T cell, B cell, NK cell. job is in the tissues |
| Granulocyte | polymorphonuclear cells. neutrophils, eosinophils, basophils |
| Basophils are what percent of WBC in circulation | 0.5% |
| Basophils contain what | granules that are filled with inflammatory mediators |
| Basophils are important in what reactions | allergy and parasitic infections. may or may not become tissue mast cells |
| eosinophils are what percent of WBC in circulation | 1-3%, half life 30 min |
| eosinophils contain what | granules that are filled with potent mediators ( eosinophilic cationic protein) capable of killing parasites |
| Where can eosinophils be found after they leave the blood | under epithelial surfaces. live in tissues for a couple of weeks and then replaced by new cells |
| eosinophils are important in controlling what | extracellular parasites. |
| Monocytes are what percent of WBC in circulation | 3-7%. circulate 1-2 days then migrate to tissue and differentiate into macrophage |
| Macrophages are important in controlling what responses | 1. phagocytosis and killing of bacteria 2. presentation of antigen of MHCII 3. secretion of cytokines TNF, IL-1, 6,12 inflammation response |
| When do monocytes/macrophages arrive at the site of infection | after neutrophils. accumulation is a sign of chronic infection |
| Neutrophils are what percent of WBC in circulation | 55-90%. short lived, 1-2 days. half life in blood 8-10 hrs. |
| Neutrophils are made where | in bone marrow |
| Role of neutrophils | 1. first to respond in bacterial infections, 4 hrs. 2. exit blood stream at the site of infection. accumulate to ingest/kill pathogen 3.Die in the process, puss |
| Neutropenia | lower than normal numbers of neutrophils in the blood stream. viral infection |
| Lymphocytes are what percent of WBS in circulation | 20-35%, circulate 4 months in blood and lymphoid tissue. look for antigen they recognize |
| What happens if a lymphocyte meets their antigen | activated and some differentiate into memory cells |
| Endothelial cells are important in what | regulating leukocytic traffic |
| Addressins | Found on endothelial cells. allow circulating leukocyte to know where they are in the body. |
| When are addressins upregulated, what does this do | during infections to facilitate binding of neutrophils to the endothelial cells. Also help find exit to site of infection |
| Granulocyte maturation | released in a mature state |
| Dendritic cell maturation | migrate to tissues and mature. Important sentinel cell and antigen presenting cells. Initiation of adaptive immunity |
| Mast cell maturation | precursors leave bone marrow and mature in tissues. live from wks to months. |
| T lymphocyte maturation | 1. released immature from bone marrow (pre T cells) 2. mature in thymus 3. T cell receptor generated by DNA rearrangement 4. if newly generated receptor recognizes antigen in thymus it is eliminated 5.If recognizes MHC then fully matures, 2nd tissue |
| B lymphocyte maturation | 1.released immature from bone marrow (pre B cells) 2. mature in bone marrow 3. Develops BCR in primary tissue 4. if BCR recognizes antigen during dev it is eliminated 5.if does not recognize antigen it matures 6. travel to 2nd tissue |
| NK cell maturation | 1.released mature from bone marrow 2. not antigen specific. no memory |
| Clonal expansion | mitosis of lymphocytes to make copies of itself |
| B cell differentiation | 1. effector plasma cells that secret AB 2. memory cells , long lived clones of cell |
| T cell differentiation | in response to antigen,differentiate into 1.effector cell 2.memory cells |
| Primary lymphoid organ for T cells | Thymus |
| Primary lymphoid organ for B cells in birds | Bursa of Fabricius |
| Primary lymphoid organ for B cells in primates, rabbits, rodents | bone marrow |
| Primary lymphoid organ for B cells in ruminants, pigs, dogs | peyer's patches |
| Secondary lymphoid organs | tonsils, spleen, lymph node, peyer's patch, bone marrow |
| Secondary lymphoid tissues does what | increases chances of lymphocyte meeting its anitgen |
| Lymph node | lymphocyte rich tissue connected to lymphatic system, where adaptive immune response to lymph-borne antigen is initiated |
| Spleen | site for adaptive immune response to blood borne antigens |
| MALT | where adaptive immune response to antigens invading from the mucosal surface is initiated |
| How do sentinel cells recognize pathogens | 1.PAMPs (exogenous) 2.DAMPs (endogenous), AKA alarmins |
| Examples of PAMPs | 1.LPS 2. Bacterial peptidoglycan 3.bacterial DNA 4. viral nucleic acids |
| Examples of extracellular DAMPs | 1. hyaluronic acid 2. heparan sulfate 3. fibrinogen 4. collagen derived peptides 5.fibronectin 6.laminin 7.elastin |
| Examples of intracellular DAMPs | 1.HMGB1 2.Uric acid 3.chromatin 4.adenosine 5.galectins 6.S100 proteins 7.cathelicdins 8.defensins 9. lactoferin 10.heat shock protein |
| HMGB-1 expression in endothelium causes | Elevated TNF, IL-8, ICAM, PA-1, VCAM |
| HMGB-1 expression in macrophages causes | elevated TNF, IL-1,6,8, HMGB1 |
| HMGB-1 expression in neutrophils causes | elevated TNF, IL-8 |
| HMGB-1 expression in DCs causes | elevated TNF, IL-1, 6,8,12 |
| HMGB-1 expression in epithelium causes | elevated iNOS |
| HMGB-1 expression in endothelium AND neutrophils causes | inflammation. Neutrophil adhesion. fibrinolysis. Causes tissue damage and shock |
| soluble PRRs | 1. collectins 2.ficolins 3.complement 4.pentraxins |
| PRRs within vessicles | TLR 3,7,8,9 |
| Cytoplasmic PRRs | 1. RIG-1 2. NOD-like 3.Peptidoglycan receptors 4.DNS receptors |
| Membrane bound PRRs | 1. TLRs 2.Lectins 3.Mannose receptor 4.Langerin 5.Dectins 6.Scavenger receptors 7.Integins |
| TLRs | transmembrane glycoprotein receptors. |
| What pathogens do TLRs recognize | bacteria, fungi, viruses |
| What TLRs do humans and cattle have | TLR1- TLR10 |
| What TLRs do mice have | TLR1-TLR9, TLR11- TLR13 |
| What are the cell surface TLRs | TLR1, 2, 4, 5,6,11 |
| What are the intracellular TLRs | TLR3,7,8,9,10 |
| What happens when a PAMP binds to a TLR | signal cascade, caspase 1 converts precursors into mature cytokines |
| Where are RIG-1 like receptors located | expressed within the cytosol |
| What do RIG-1 like receptors recognize | viral dsRNA |
| What happens once a RIG-1 like receptor is activated | activate caspase and trigger signaling pathways. Production of IFN-1 |
| Where are NOD like receptors located | within the cytosol |
| What does NOD1 recognize | bacterial peptidoglycans |
| What does NOD2 recognize | muramyl dipeptide and serves as a general sensor of intracellular bacteria |
| What does activating a NLR activate | NK-B pathway. production of proinflammatory cytokines |
| what does NOD2 specifically activate | the production of defensins |
| inflammation | a tissue reaction that rapidly delivers mediators of host defense to the site of infection and tissue damage |
| what are the three essential roles of inflammation | 1. delivers additional effector molecules and cells to sites of infefction to augment the killing of invading microbes by the front line macrophages 2. provide a physical barrier preventing the spread of infection 3. promote the repair of injured tissue |
| what is the MAIN purpose of inflammation | focus the immune response to the site of infection or injury |
| CXCL8 (IL-8) | chemokine produced by macrophages or mast cells. attracts and activates neutrophils |
| CXCL2 | chemokine secreted by macrophages and attracts neutrophils |
| what are the three major cytokines that sentinel cells synthesize and secrete when exposed to PAMPs or DAMPs | TNF-a, IL-1, IL-6 |
| TNF-a, IL-1, IL-6 expression in liver causes | acute phase proteins and activation of complement opsonization |
| TNF-a, IL-1, IL-6 expression in bone marrow causes | neutrophil mobilization and phagocytosis |
| TNF-a, IL-1, IL-6 expression in hypothalamus causes | increased body temperature leading to decreased viral and bacterial replication, increased antigen processing, facilitates adaptive immune response |
| TNF-a, IL-1, IL-6 expression in Fat/muscle causes | protein and energy mobilization to generate increased body temp leading to decreased viral and bacterial replication, increased antigen processing, facilitates adaptive immune response |
| TNF-a, IL-1, IL-6 expression in DCs causes | TNF-a stimulates migration to lymph nodes and maturation therefore initiating adaptive immune response |
| why is a fever stimulated | hypothalamic response to cytokines. muscle and adipose cells alter energy mobilization to generate heat |
| effects of fever/heat | 1. bacterial and viral replication decreased at high temp 2. antigen processing enhanced 3.adaptive immunity becomes more potent 4. cells become more resistant to neg effects of TNF-a |
| stages of neutrophil adhesion and emigration from blood vessels | 1. rolling 2. adherence 3. migration 4, emigration/ diapedesis 5. chemotaxis |
| Rolling of neutrophils is mediated by what PAMPs/DAMPs | selectin mediated |
| Adherence until diapedesis is mediated by what PAMPs/DAMPs | integrin mediated |
| Elastase | anti adhesive molecule. allows neutrophils to enter tissues |
| in neutrophil adhesion and emigration what are the specific selectins | L- selectin, p-selectin |
| in neutrophil adhesion and emigration what are the specific integrins | LFA-1 and ICAM-1 |
| Cardinal signs of inflammation | redness, swelling, heat, pain |
| what is redness caused by | increased blood flow to the area of injury |
| what is swelling caused by | increased extravascular fluid and phagocyte infiltration to the damaged area |
| what is head caused by | increased blood flow and the action of pyrogens |
| what is pain caused by | local tissue destruction and irritation of sensory nerve receptors |
| Histamine | most important vasoactive molecule released by mast cells. |
| what happens when histamine binds to its receptor on endothelial cells | stimulates them to produce NO (potent vasodilator) |
| What does histamine cause | blood vessel leakage, leading to fluid escape into tissue and local edema. up-regulates TLR expression on sentinel cells |
| Serotonin chemically known as | chemically 5HT, derivative of tryptophan. |
| What does serotonin do | normally causes a vasoconstriction that results in a ride in blood pressure |
| C5a and C3a | complement proteins. promote histamine release from mast cells. |
| What do kallikreins act on | kininogens to generate kinins |
| Bradykinin | the most important kinin. Increase vascular permeability, stimulate neutrophils and trigger pain receptors |
| coagulation system | large amount of thrombin generated. |
| What does thrombin act on | fibrinogen in tissues and plasma to form insoluble fibrin |
| where is fibrin deposited | in the inflammed tissue forming a physical barrier to the spread of infection |
| what does the fibrinolytic system do | destroys fibrin and releases peptide fragments that attract neutrophils |
| Steps of phagocytosis | 1. chemotaxis 2. adherence 3. ingestion 4.destruction |
| chemotaxis | delivery of phagocytic cells to the site of infection |
| Adherence | phagocytic adherence to the target |
| ingestion | engulfment of the target particle |
| destruction | intracellular killing and digestion of the target |
| Opsonization | coating of a hydrophilic material with opsonins. IgG, IgM, C3b |
| what does opsonization of a hydrophililic particle allow | the neutrophil to bind to it |
| what are the types of neutrophil membrane receptors | 1. Fc receptors 2. C3b receptors |
| Fc receptors | bind AB that is bound to an antigen. esp IgG |
| C3b receptors | bind to C3b when it is coating bacteria |
| Phagosome | membrane bound vesicle containing the ingested microbe or material |
| what does the phagosome have to bind to for the ingested particles to be destroyed | lysosome. forming a phagolysosome. |
| why is the killing process confined to the phagolysosome | so that the toxic substances and lethal activities of the phagocytes can't harm itself. |
| what are the three killing processes of intracellular pathogens | 1. lytic enzymes antimicrobial peptides from granules 2. oxidative metabolism 3. neutrophil extracellular traps |
| Hydrolases | break covalent bonds by adding water. |
| when are hydrolases important | for degrading dead bacteria or dead tissue |
| lysozyme | breaks down peptidoglycan in Gram-pos bacteria |
| defensins | small cationic proteins that kill bacteria, esp Gram-pos. hydrophobic outside and hydrophilic interior to insert into a membrane= pore |
| myeloperoxiase | important rose in the oxygen mediated killing mechanism |
| lactoferrin | chelates iron that bacteria need for survival |
| collagenase | degrades connective tissue so it can move through to the site of inflammation |
| where does oxygen mediated killing occur | in the phagolysosome |
| what are the killing products of respiratory burst | 1. hypochlorite 2. hydrogen peroxide 3.aldehydes 4.oxygen radicals |
| what are NETs stimulated by | CXCL8 or LPS. |
| How are NETs produced | when neutrophils release nuclear material and granular proteins extracellularly |
| NETosis | an active response to inflammatory stimuli |
| Macrophages in the lung are called | Alveolar macrophages |
| Macrophages in the liver are called | Kupffer cells |
| Macrophages in the bone are called | osteoclast |
| Macrophages in the spleen are called | Splenic macrophages |
| Macrophages in connective tissue are called | Histiocyte |
| Macrophages in the brain are called | microglia |
| when are M1 macrophages activated | in the innate activation. |
| What do M1 macrophages induce | increased 1.size 2.movement 3.membrane activity 4.lysosomal enzymes 5.phagocytosis 6. bactericidal activity 7.MHC class II expression 8. NO production |
| When are M2 macrophages activated | during the alternate activation pathway |
| what do M2 macrophages induce | 1. Increased tissue repair 2.increased MHC class II expression 3.Reduced microbial killing |
| what is the role of macrophages in chronic infections | induce fibrosis and granuloma formation |
| complement | a group of serum and cell surface proteins activated by the combination of antigen and AB. |
| what does the general activation of complement lead to | the generation of enzyme cascades that have a variety of actions including cell lysis and opsonization |
| what are the main functions of the complement system | 1. bacterial lysis (complement mediated cytolysis) 2. opsinozation and phagocytosis 3. inflammation |
| the larger complement fragment generally acts as what | an enzyme to activate the next protein in the cascade. "b" |
| the smaller complement fragment generally acts as what | is released and may influence a separate process. "a" |
| Alternate pathway | pathogen surface creates local env conductive to complement activation. first to act |
| lectin pathway | mannose binding lectin binds to pathogen surface. second to act |
| classical pathway | c reactive protein or AB to specific antigen on pathogen surface. Third to act |
| what does the general activation of C3a, C4a, and C5a lead to | recruitment of inflammatory cells |
| what does the general activation of C3b lead to | 1. opsonization of pathogens, phagocytosis 2. MAC formation |
| what is the merge point of the classical, MBL, and alternative pathway | C3 convertase where C3 is divided into a and b subunits |
| classical and MBL C3 convertase | C4b2b |
| Alternative C3 convertase | C3bBb |
| initiation of the classical pathway | 1. when AB binds antigen there is a conformational change in the Fc portion of AB 2. allows C1 to bind to the Ag-Ab complex. there must be 2 Fc binding sites for C1 to bind. |
| What AB are required for classical pathway initiation | one IgM or two IgG. IgM more efficient |
| when is C1 activated | when it binds the Fc region of an AB |
| What is C1 | the protease that cleaves the next 2 components of the classical pathway C4 and C2 |
| what is Cb3 | an opsonin |
| MAC | formation of a transmembrane pore. results in lysis and cell death |
| how is complement activation regulated | 1. C1-INH 2.CD59 |
| C1-INH inhibits what | can't make C3 convertase |
| CD59 inhibits what | final assembly of the MAC at the C8 to C9 stage |
| Factor H and Factor I | blocks formation of MAC |
| In general what happens when C2a is activated | increase in vascular permeability |
| In general what happens when C3b is activated | immune regulation and opsonization |
| In general what happens when C5b67 is activated | leukocyte chemotaxis |
| In general what happens when C3a is activated | Anaphylatoxin and microbial killing |
| In general what happens when C5a is activated | 1. Neutrophil chemotaxis 2. anaphylatoxin 3.lysosomal enzyme secretion 4. neutrophil activation 5. increased vascular permeability 6. smooth muscle contraction |
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ejohnson17
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