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IMS > Immunology > Flashcards

Immunology Flashcards

1
Q

what is the innate immune system

A

first line of defence, non-specific response, no memory, present from birth

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2
Q

what is the difference between active and passive immunity

A

active - antigens enter body and trigger innate/ adaptive system - provides long term treatment
passive - antibodies pass from mother to foetus across placenta/breast milk provides short term protection

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3
Q

what are some mechanical barriers

A

skin, mucous, normal flora, cilia

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4
Q

what are some physiological barriers

A

stomach acid, fever response inhibits growth

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5
Q

what are chemical mediators in the innate response

A

plasma proteins, lysosome cleaves bacterial cell wall, interferon induces antiviral defences in uninfected cells, complement lyses microbes directly facilitates phagocytosis

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6
Q

what are some examples of phagocytic leukocytes

A

phagocytes (specialised cells in phagocytosis)
macrophages (reside in tissues and recruit neutrophils, actuated by cytokines
neutrophils (enter infected tissues in large numbers and cause release of cytokines and phagocytose bacteria

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7
Q

what are NK cells

A

natural killer cells summoned from blood, release cytokines and kill infected cells via causing apoptosis

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8
Q

what is the main function of the compliment system

A

they form membrane attack complexes which attack pathogens

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9
Q

what molecules are produced by the complement pathway

A

anaphylatoxins - by products from complement factors which play a role in allergic reactions nd anaphylactic shock

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10
Q

how do the complement system aid in phagocytsis

A

helps prime pathogens for macrophages and neutrophils and attract them to the site of infection

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11
Q

how is the classical pathway of the complement system activated and what does it involve

A

activated by antigen - antibody complexes - triggered second by exposure to pathogen, serine proteases, involves limited proteolysis to activate next factor and there is amplification
the first step is complement factor c1 binding to antigen/antibody complex

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12
Q

describe the mechanism of the classical pathway of the complement system

A
  • Step 1 = C1 cleaves C2 into C2a and C2b
  • Step 2 = C1 also cleaves C4 into C4a and C4b
  • Step 3 = C2a and C4b form complex cleaving C3 into C3a and C3b
  • Step 4 = C3b joins C2a/C4b complex forming C2a/C4b/C3b complex cleaving C5 into C5a and C5b
  • Step 5 = C5b finally forms complex with C6, C7, C8 and C9 producing membrane-attack complex to perforate cell membranes
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13
Q

describe the process of the lectin mannose binding pathway

A

Activated first, directly by pathogens, involves mannose-binding lectin which binds mannose found on surface of pathogens but not mammalian cells
MBL binds MASP 1 and 2 (mannose associated serine protease) which activate C2 and C4
Rest of pathway the same

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14
Q

describe the process of the alternative pathway

A

Activated first, direct contact with pathogens
Autoactivation of C3 into C3a and C3b, occurs constantly at low rate
Upon contact with pathogen autoactivated C3b binds factor B and properdin which rapidly activates more C3 and activates C5
Rest of pathway same

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15
Q

what is the role of the by products C3a, C4a and C5a

A

they are anaphylaxtoxins, trigger degranulation of endothelial cells, mast cells and phagocytes
the also cause smooth muscle contraction and enhance vascular permeability

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16
Q

C3a and C5a are chemoattractants what does this mean

A

attracts and activate neutrophils

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17
Q

C3b causes opsonisation - what does that mean

A

pathogens labelled, C3b renders bacteria more susceptible to phagocytes, C3b cleaved to iC3b on bacterial surface, macrophage cell membrane contains receptors for iC3b, facilitating phagocytosis of bacteria by macrophage

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18
Q

what do all cells in the immune system arise from

A

common pluripotent hematopoietic stem cells in the bone marrow

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19
Q

what cells make up the myeloid lineage

A

polymorphonuclear leukocytes such as neutrophils, eosinophils and basophils

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20
Q

what is an eosinophil

A

defender against multicellular parasites and allergy / asthma

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21
Q

what are neutrophils

A

principal phagocyte of innate immune system - migrate to site of infection ingest microbes by phagocytosis and release o2 free radicals - degranulate releasing proteins with microbicidal properties eg lysozyme

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22
Q

what is a basophil

A

inflammatory allergic reaction releases histamine vasodilator

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23
Q

what is a monocyte

A

circulate, bean shaped nuclei, precursors of tissue macrophages, effectors of inflammatory response to microbes, kills pathogen via phagocytosis - produces free radicals and inflammatory cytokines

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24
Q

what do macrophages do

A

derived from blood monocytes - involved in innate and active immunity - phagocytosis, microbicidal mechanisms and presents antigen to other cells

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25
Q

what is the role of dendritic cells

A

antigen presenting cells which process and present antigens on cell surface to T cells to initiate specific responses

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26
Q

what is the role of mast cells

A

similar to basophils - release histamine - association with allergy and inflammation

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27
Q

which cells make up the lymphoid lineage

A

B and T cells

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28
Q

what do B cells do

A

produce antibodies , present antigens and can produce memory cells

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29
Q

what is the role of T cells

A

development and regulation of cell mediated immunity, influences activities of other cells, kill virally infected cells and tumour cells - generate long lived memory cells

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30
Q

what is the role of natural killer lymphocytes

A

part of innate response - release perforins and granzyms and trigger apoptosis of target cells - kill cells infected viral cells and ones which do not express foreign surface antigen - involved in tumour immunosurveliiance

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31
Q

what are the professional phagocytes

A

macrophages, dendritic cells, neutrophils (NK cells use a different mechanism)

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32
Q

how does phagocytosis work

A

pathogens engulfed by cell membrane forming phagosome
phagosome fuses with lysosome containing digestive enzymes which forms a phagolysosome which digest the pathogen
material is then secreted by fusion with the cell membrane

33
Q

what are macrophages commonly found

A

lungs, under the skin and around intestines

34
Q

describe the 3 activation stages of a macrophage

A 
Activation state 1 = resting = collects debris from tissues by phagocytosis, eliminates apoptotic cells, expresses little MHC class II on membranes
Activation state 2 = primed macrophage = primed with cytokine INF-gamma produced by NK cells and Th cells, primed macrophages express increased levels of MHC II, take up larger objects by phagocytosis
Activation state 3 = hyper-activated = macrophages become hyperactive when stimulated with both INF-gamma and lipopolysaccharide produced by gram-negative bacteria, stop proliferating, become larger and increase rate of phagocytosis, produce cytokines (tumour necrosis factor) and interleukin-1 which can kill tumour/virus cells
35
Q

what is expressed on neutrophils to allow them to circulate freely

A

SLIG compared to an endothelial cell which has ICAM

36
Q

what are released by macrophages when a tissue becomes infected

A

cytokines, IL-1 and TNF

37
Q

what do cytokines stimulate in terms of endothelial cells and neutrophils

A

expression of selection on endothelial cell membrane which SLIg on neutrophil binds this interaction causes cell to bind and start rolling on endothelium

38
Q

what is the role of intergrin in neutrophil rolling

A

binds to ICAm expressed on the endothelium - now neutrophil-endothelium interaction is strong - cell stops rolling and sticks to vascular wall close taste of infection

39
Q

how are neutrophils able to track bacterial proteins

A

neutrophils have Met amino acid at N terminal but bacteria have f-met so can use to track them

40
Q

how specifically to neutrophils enter the site of infection

A

under C5a influence and bacterial f-Met peptides the neutrophils infiltrate the endothelium and inflamed tissues surrounding vessel

41
Q

once a neutrophil has entered a site of infection what happens to it

A

they become extremely phagocytic and produce TNF cytokines to activate other immune cells - they are short lived though and they are the puss as infected site

42
Q

what lineage to NK cells come from

A

lymphoid lineage

43
Q

what is the mechanism of action of a NK cell

A

produced in bone marrow and mainly found in blood/liver/spleen
they also travel to site of infection and release cytokines
destroy infected cells by apoptosis
use Fas ligand to bind to target cell doesn’t attack normal cells as they have MHC-1
they use perforin protein to inject granzyme B into cell

44
Q

what is the difference between humeral and cell mediated response

A

humoral is mediated by antibodies and produced by B cells

cell mediated is induced by T cells

45
Q

what do white blood cells do when there is no site of infection

A

resident macrophages eat dying cells - dendritic cells on sentry duty waiting for first sign of pathogen - most monocytes and neutrophils pass by in the blood stream

46
Q

what occurs in the adaptive immune system upon first wave of infection

A

dendritic cells exit infected tissues to inform lymphocytes in lymph nodes about invading pathogen - neutrophils also move from blood into the infected site

47
Q

what is the second wave of infection

A

neutrophils have killed pathogen but also killed themselves making pus - monocytes enter site and remove debris

48
Q

what is the role of inflammatory macrophages

A

help repair damaged tissue

49
Q

where to b cells come from

A

bone marrow

50
Q

what is the role of a B cell

A

antibody production - activation of T cells and innate immunity complement system

51
Q

where do T cells come from and what is their role

A

from the thymus and matured in the bone marrow - produce cytokines
T cells need antigens presented otherwise they cannot recognise them - these can be presented by monocytes/macrophages/b cells/dendritic cells etc
they kill directly after direct interaction

52
Q

what is the difference between CD4 and CD8

A

CD4 is helper cell and CD8 is cytotoxic

53
Q

what is the difference between Tc cells and Th cells

A

Th cells help activate B cells and activate phagocytes

Tc - cytotoxic, effective at attacking viruses, attack cell and virus inside cell

54
Q

what are the three types of T cell

A

regulatory
cytotoxic
helper

55
Q

describe the process of B cell activation

A

Antibody-antigen interaction not enough to activate B cells and second signal needed – T cells
Overall need interaction between B, T cells and non-immune response

56
Q

describe the what happens in B cell maturation

A

Maturation is clonal expansion, production of huge amounts of antibody
Plasma cell mature version of B cell, after has been activated, each specific B cell proliferates to produce clone of identical cells, plasma cells produce large amounts of antibody

57
Q

why are B cells called memory cells

A

B cells remember an antigen, if confronted on second occasion, antibody response much quicker and larger (vaccination method), plasma cells die off after few weeks but some remain as memory cells, enables pathogen to be quickly dealt with

58
Q

how to B cells activate T cells

A

B cells act as antigen presenting cells, stimulating T cell arm of immune system, interaction between B and T cells crucial for healthy immune response, T cells require B cells to present antigen to stimulate T cells

59
Q

describe the process of t cell activation

A

Antigen processed and presented in conjunction with MHC class I or II T cells
Second signal is needed, otherwise T cell fails to be activated and doesn’t respond
Second signal comes from recognition of CD28 molecule on T cell by CD80 molecule on APC cell
Prevents T cells being activated by body’s own antigens

60
Q

what happens when a T cell is activated

A

Causes cytokine production – chemoattraction, autoactivation, augmentation of inflammation, stimulation of antibody production by B cells, activates non-specific response, MHC II/CD4
Causes cellular death = MHC1/CD8

61
Q

what are MHC molecules

A

Major histocompatibility complex glycoproteins present on cell surfaces to help differentiate self from non-self

62
Q

what is the relation between T cells and MHC molecules

A

T cells only recognise antigens as complexes with MHC molecules, role in T cell activation

63
Q

how to MHC help normal cells from immune system

A

Peptides present on surface of antigen presenting cells with MHC, allows immune cells to discriminate between normal antigens on surface of all cells and those foreign and potentially dangerous

64
Q

what is the role of MHC1 molecules

A

proteins present on almost every cell in body, present endogenous antigens synthesised in cytoplasm, samples of all proteins made on ribosomes, whether normal host proteins chopped up into short peptides on proteasome, resulting peptide fragments transported into ER, peptides about 10 amino acids can bind to MHC 1 proteins, peptide MHC complexes transported via golgi to cell surface, once at surface membrane bound MHC 1 protein displays antigen for recognition to cytotoxic T cell lymphocytes (CD8+), if foreign protein fragments detected, cell is killed

65
Q

what is the role of MHC class 2 molecules

A

proteins only present on specialised antigen-presenting immune cells/macrophages/dendritic cells/B cells, proteins present exogenous antigens that originate extracellularly from foreign bodies e.g. bacteria, following phagocytosis, foreign peptide fragments bound to MHC 2 proteins in endosome, before being transported to cell surface, once at cell surface, membrane bound MHC 2 protein displays antigen, recognised by different type of T cell, helper T cell lymphocyte (CD4+), binding of helper T cells to B cell MHC 2-antigen stimulates development of antibody producing B cells against antigen

66
Q

describe the process of MHC antigen presentation

A

antigen processed after being taken up by cell, antigen presented with MHC, MHC present on all cells and specific, viral antigens presented with MHC I molecules to T cell by infected cell, so Tc cells kill infected cell, APC cells present foreign peptide together with MHC II to T helper cells, do not kill APC but release cytokines to trigger immune response

67
Q

describe the process of T helper cell activation

A

antigen presenting cell ingests antigen, breaks down into peptides, APC presents peptides with MHC class II molecules on surface, combination recognised by T helper cells with CD4 protein, resting T helper cell now activated and releases cytokines which signal other cells to boost response of immune system to invading pathogen

68
Q

describe the process of T cytotoxic cell activation

A

cell infected with virus will process virus to produce peptides, peptides loaded onto MHC I molecule in ER and transported to cell surface, presented to T cytotoxic cell with CD8 receptor, T cytotoxic cells kill infected cell, so preventing virus being reproduced

69
Q

what are the 5 immunoglobulins

A

a, g, d, e, m

70
Q

what are immunoglobulins structure eg IgG

A 
made from a light chain and heavy chain
Two identical antigen binding regions, Fab (variable region) making it specific, due to folding which matches shape of antibody (top parts – two recognition sites)
Tail region (constant) can bind to receptors on surface of cells such as macrophages
71
Q

what are the two types of cell a B cells forms

A

plasma cells produce antibody to fight infection,

memory cells survive in blood stream so if antigen encountered again are more cells ready to respond

72
Q

how are antibodies specific

A
  • Antigen binding site has to be perfect fit for antigen, antibodies ambush antigens in blood stream or interstitial tissue, unable to enter cells, important as viruses enter cells so antibodies cannot access virus until cell dies, each B cell makes specific antibody (monoclonal), B cells transformed into plasma cells to produce antibodies
73
Q

what is the structure and role of IgM

A

pentamer = main antibody of primary responses, mainly in blood stream fixing complement, serves as B cell receptor (transmembrane domain so not released from cell), slow rise in primary response, limited rise in secondary response, kills bacteria, first to arrive after pathogen encounter

74
Q

what is the structure and role of IgG

A

monomer = main antibody of secondary responses, major in the blood, enters tissue space, neutralises toxins, opsonization (prepares bacteria to be killed), Fc binds to phagocytes, slow rise after IgM in primary response, rapid rise in secondary response

75
Q

what is the structure and role of IgA

A

secretory dimer = secreted into mucus, tears, saliva, colostrum, protects entrance of pathogens

76
Q

what is the difference between IgE and IgD

A

IgE monomer = antibody of allergy and antiparasitic activity, Fc binds to mast cells and basophils, trace amount
IgD monomer = B cell receptors, transmembrane domain so not released from cell, found in B cell membrane, helps cell division

77
Q

how does immunisation work

A 
Life attenuated (weakened) virus, killed virus, part of virus
Immune response develops and provides long-lasting immunity (memory B cells and IgG antigens)
Booster injections may be required, memory can fade
78
Q

what is class switching and why does it occur

A

B cells can change type of antibody produced, called class-switching, IgM shows recent infection, mainly in bloodstream, later immunity is high IgG, in blood and interstitial tissue, can remain for years in the blood so doesn’t always mean recent infection

IMS (20 decks)

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