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exam 2

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
Created by: ejohnson17



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