Immunology Flashcards Preview

DENT 291 > Immunology > Flashcards

Flashcards in Immunology Deck (59):
1

Define attenuation

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

2

how can attenuation be achieved?

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

3

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

4

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

5

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

6

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

7

what is plasma?

the cell-free component of blood

8

what is serum?

plasma, without clotting factors

9

what is passive immunization?

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

10

what is active immunization?

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

11

what is an antigen?

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

12

what is the epitope?

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

13

what is cross-reaction?

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

14

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

15

what are mononuclear cells?

contain one nucleus
monocytes, macrophages, and dendritic cells

16

what cells act as phagocytes?

neutrophils, macrophages, and dendritic cells

17

which cells of the immune system are APCs?

macrophages and dendritic cells--so the monocytes

18

what are a macrophages effector functions?

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

19

what act as macrophages in the liver?

kupffer cells

20

what act as macrophages in the CNS?

microglial cells

21

what act as macrophages in bone?

osteoclasts

22

what act as macrophages in the lung?

alveolar macrophages

23

how are macrophages activated?

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

24

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

25

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

neutrophils; have effector mechs similar to macrophages

26

mast cells effector mechanism?

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

27

what activates mast cells?

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

28

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)

29

what recruits and causes differentiation in eosinophils?

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

30

dendritic cells stop phagocytic activity and increase MHC II once mature

ye

31

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

ye

32

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

33

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

34

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

35

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

36

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

37

examples of PAMPs?

dsDNA
LPS, lipopolysaccharide
flagella
fungal cell wall

38

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)

39

what is the first line of defense in humans?

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

40

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

41

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

42

what are the functions of complement?

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

43

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

44

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;

45

what is leukocyte infiltration?

presence of more leukocytes than normal

46

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

47

what are the important cytokines in inflammation?

IL-1, 6, and TNFa

48

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

ye

49

what are pyrogens, and what chemicals act as them?

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

50

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

51

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

52

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

53

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

ye

54

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

55

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

56

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

ye

57

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

ye

58

basophils-“A circulating mast cell”

ye

59

eosinophils--contain major basic protein

ye