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Flashcards in Immunology Deck (59):

Define attenuation

the process of decreasing virulence of pathogens
does not include killing pathogens, just making them weaker


how can attenuation be achieved?

growing culture under non-optimal conditions
passage of pathogen through other species


what are the characteristics of the immune system (both innate and adaptive)

1. Specificity
2. Universaility
3. Positive memory--rxn stronger with next exposure of particular antigen
4. Self-nonself discrimination
5. Immune class regulation


what is a cytokine?

a molecule excreted by one cell that acts on another cell-->binds to cytokine receptor on target cell; used for cell-cell communication


what is a chemokine?

a chemotactic cytokine-->attracts cells to the site where the chemokine is produced--target cells have chemokine receptor; important in cell recruitment


what is a cluster of differentiation?

molecules expressed on the surface of cells that can be used to identify different types of cells
--there are different CDs with different functions


what is plasma?

the cell-free component of blood


what is serum?

plasma, without clotting factors


what is passive immunization?

transfer of immunity to a "naive" person via transfer of serum or cells


what is active immunization?

vaccination--> inducing host's OWN immune response to produce Abs via either attenuated or "dead" pathogen


what is an antigen?

the molecule/protein/etc being recognized by the immune system


what is the epitope?

the particular part of the antigen that the Ab/receptor of the immune system binds to


what is cross-reaction?

when one antigen shares at least one epitope with another antigen such that an immune response in recruited


what is a granulocyte/polymorphonuclear cells, and what are the different types?

cells that contain granules in cytoplasm and and have nuclei with odd shapes and are multisegmented;
e.x. eosinophils, basophils, neutrophils, and mast cells


what are mononuclear cells?

contain one nucleus
monocytes, macrophages, and dendritic cells


what cells act as phagocytes?

neutrophils, macrophages, and dendritic cells


which cells of the immune system are APCs?

macrophages and dendritic cells--so the monocytes


what are a macrophages effector functions?

phagocytosis; ROI (reactive oxygen intermediates), RNIs (reactive nitrogen intermediate)-- ROIs/RNIs are very damaging to whatever macrophage ate


what act as macrophages in the liver?

kupffer cells


what act as macrophages in the CNS?

microglial cells


what act as macrophages in bone?



what act as macrophages in the lung?

alveolar macrophages


how are macrophages activated?

PAMPs; pro-inflammatory cytokines; Abs, Cb3, interferon gamma; after activation, their effector functions increase and upregulate the MHC II


what is opsonisation and what are the opsonins?

flagging an antigen/pathogen for ingestion by phagocyte which will make the antigen/pathogen more likely to be ingested
Abs and Cb3 component of complement


what is the first cell to be recruited to a site of inflammation?

neutrophils; have effector mechs similar to macrophages


mast cells effector mechanism?

granules containing pro-inflammatory mediators such as IL-5, IL-4, IL-13, and histamine


what activates mast cells?

pressure nerve cells (they are tissue resident)
IgE bound to Ag (mast cells contain FcR)
C5a-->triggers degranulation


what does eosinophilia indicate?

increased levels of eosinophils; usually means parasitic infection because eosinohpils produce major basic protein in their granules-->damaging to parasites
(doesn't always mean this though)


what recruits and causes differentiation in eosinophils?

IL-4, IL-5, as released by mast cells


dendritic cells stop phagocytic activity and increase MHC II once mature



dendritic cells contain PRRs--.bind to PAMPs; they sample the enviro and report back to lymph cells where the adaptive immune system is activated



NK cell effector function?

cytotoxic--have perforin and granzyme B
perforin--protein that perforates cell membranes-->cytoplasm leaks out
granzyme B--diffuses through hole created by perforin and triggers apoptosis in the cell


how do NK cells differentiate between healthy and unhealthy cells?

NK cells contain activating and inhibiting receptors
all cells contain activating or inhibiting signals
--NKs receive BOTH of these signals; the balance between them determines whether or not NKs will target that cell
A stress/infected/tumor cell will either have: an INCREASE in ACTIVATING signals OR a DECREASE in INHIBITING signals which will then activate the NK cells


what are some examples of activating signals for NK cells?

Atibodies on target cell-> stimulte antibody dependent cell mediated toxicity;
stress signals (eg MIC-A and MIC-B)-->MHC I-like molecules found on tumor cells and virally infected cells


what are some inhibiting signals for NK cells?

MHC I molecules
if they start to disappear from the cell surface, something is wrong-->decrease in inhibitory cells-->activates NK cells


what are PRRs?

pattern recognition receptors
recognize pattern associated molecular patterns which are usually conserved molecules present on pathogens
are expressed on many cell types, especially APCs


examples of PAMPs?

LPS, lipopolysaccharide
fungal cell wall


why are PAMPs being included into adjuvants in vaccines?

because if a PAMP binds to a PRR-->then you get an even stronger immune response (both innate and adaptive)


what is the first line of defense in humans?

barriers--physical (skin, mucosa) and chemical (acid, lysozyme)


what are AMPs, what produces them?

antimicrobial peptides; Produced by epithelial cells as well as some leukocytes (such as NK cells and neutrophils and CTLs)
Example: Defensins
Short polypeptides
Cause direct cytotoxicity on microbes (bacteria and fungi)
Activate cells involved in inflammatory response


describe the complement pathway

the complement cascade is activated; some components are cleaved and give rise to a and b complement components; a is soluble, b is sticky--help to hold complement proteins onto the pathogen-->insert membrane attack complex


what are the functions of complement?

opsonization--C3b (sticky) sticks onto cells--macrophages smell it
chemotxis--C5a (soluble)
inflammation (C3a and C5a)


what are the 3 complement pathways?

Classical pathway--activates upon surface coated with antibodies; C1 components form complex that recognize Abs and bind to pathogen;
Alternative pathway--C3 can be cleaved spontaneously; we have mechanisms to (negative feedback) which detabilizie the spon. cleavage; but pathogens do not
Lectin pathway--mediated by mannan binding lectin--not found on our cells;

all 3 pathways converge on the cleavage of C3, just activation that differs


what is inflammation?

the process of recruitment of leukocytes and plasma proteins from the blood, their accumulation in tissues and their activation in the tissue to destroy microbes--recruitment important, the cells and proteins must concentrate in an area to be effective;


what is leukocyte infiltration?

presence of more leukocytes than normal


what are the steps of inflammation?

1. tissue damage-->leads to release of cytokines from tissue cells, mast cells, and macrophages
2. chemokines attract leukcytes to site of damage/infection etc
3. cytokines cause vasodilation-->more nutrients, increased leakiness for more cells to come through
4. increased leakiness means more cells can enter via paracellular transmigration; proteins from blood (e.g. Abs, complement components) can enter
5. newly immigrated cells can produce more recruiting mediators
dendritic cells in the tissues take up antigens and report back to lymph nodes-->activate adaptive immune system
antigens can also flow into "draining" lymph nodes and initiate adaptive immune system on their own without dendritic cells


what are the important cytokines in inflammation?

IL-1, 6, and TNFa


Pro-inflammatory cytokines:
Produced by a variety of cell types
Mast cells, macrophages?
Production increased in presence of PAMPs
Can also act as chemokines (TNFa and IL-1)
Act on postcapillary venules to increase expression of homing signals (by TNFa and IL-1)
Stimulate neutrophils production in bone marrow
Basically, they promote inflammation



what are pyrogens, and what chemicals act as them?

increae body temp by acting on hypothal-->fever
IL-1, 6 and TNFa


what are interferons?

molecules which interfere with viral replication
Increase production of proteins that block viral transcription and translation
Upregulate expression of Class I MHC
Increase sensitivity to apoptosis


roles of epithelia

Role of epithelium:
At skin, they form tight junctions and produce keratin
At mucosal surfaces, they produce mucus
Mucous prevents colonization ofpathogens on tissue
Produce antimicrobial peptides (AMPs):
Produced by epithelial cells as well as some leukocytes (such as NK cells and neutrophils and CTLs)
Example: Defensins
Short polypeptides
Cause direct cytotoxicity on microbes (bacteria and fungi)
Activate cells involved in inflammatory response


define inflammation

Inflammation is the process of recruitment of leukocytes and plasma proteins from the blood, their accumulation in tissues and their activation in the tissue to destroy microbes


IL-1, IL-6 and TNFa:
Act as pyrogens:
Act on hypothalamus increase production of prostaglandins  fever
Inhibited by NSAIDs (like aspirin)
Act on (BIND TO) liver to produce acute phase reactants
C-reactive protein (CRP)
Can be requested as part of blood analysis to indicate presence of inflammation
Fibrinogen (causes elevated ESR  another marker for inflammation)
Can also measure in blood analysis
Measure indirectlyleave serum sitting, measure how long pptation of cells takesif it is quick, lots of clotting factorslots of inflammation
Involved in clotting



consequences of TFN-a?

cause the following:
Decreases vascular tone drop in blood pressure  shock (ex: septic shock)
septic shock = severe inflammation that occurs in the blood
Increases production of tissue factor  increases thrombosis (you will learn about tissue factor next term)
Suppresses appetite  wasting of muscle and fat cells (this is known as cachexia)
Sometimes, inflammation/clotting can occur in the periphery can begin to lose limbs


what are IFNs, what are they for, how are they produced and by what?

Interfere with viral replication Play a very important role in antiviral response
Increase production of proteins that block viral transcription and translation
Upregulate expression of Class I MHC
Increase sensitivity to apoptosis
IFNa, IFNb (and IFNg)
Produced in response to recognition of viral nucleic acids (through PRR’s)
Produced by infected cells to act on other cells to prevent spread of infection


IL-1, 6, and TNF-a acts as pyrogens, and also bind to liver receptors to create C-reactive protein and fibrinogen



mast cells:

Play a role in allergies
Play a role against helminths infection
Increase peristalsis and mucus
Increase in peristalsiscleans out GI
Increase in mucus prevents colonization



basophils-“A circulating mast cell”



eosinophils--contain major basic protein