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Year 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

Physical infection barriers

A
  • skin + mucosal membranes
  • tight junctions between cells prevent pathogen entry
  • flushing action of tears, saliva + urine
  • high oxygen tension in lungs
  • mucus traps microorganisms + is expelled by coughing, sneezing + cilia
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2
Q

Chemical infection barriers

A
  • acidic pH (stomach + vagina)

- lysozyme + pepsin destroy microorganisms

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3
Q

Biological infection barriers (normal flora)

A

non-pathogenic bacteria colonise on epithelial surfaces

  • competes with pathogenic bacteria for nutrients + space
  • produces antibacterial substances
  • antibiotics can disrupt normal flora
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4
Q

Phagocytes function

A
  • macrophages + neutrophils
  • engulf + destroy pathogens (phagocytosis)
  • upon infection, macrophages release cytokines that recruit neutrophils
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5
Q

Neutrophils

A

migrate from bloodstream in response to tissue damage, complement proteins + chemicals released by macrophages

  • can be activated + recruited by interleukin-8 (IL-8) and tumour necrosis factor (TNF) [secreted by macrophages] or by IL-17 [secreted by T cells of adaptive immune system]
  • act by phagocytosing invading organisms + presenting antigens to immune system
  • segmented nuclei + cytoplasm contains pinky-purple intracellular granules
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6
Q

Macrophages

A
  • phagocytose + destroy pathogens + cancer cells
  • tissue cells (not found on FBC)
  • opsonins can increase rate of phagocytosis (eg IgG + complement protein C3b) [neutrophils + macrophages may have receptors for opsonins which may be on antigenic surface)
  • stimulate response of other immune cells
  • pseudopodia = processes on cell membrane which extend around pathogen
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7
Q

MAMPs + PAMPs

A

microbe associated molecular patterns
pathogen associated molecular patterns
MAMPs and PAMPs recognised by toll-like receptors
toll-like receptors are found at plasma membranes and in phagosomes and they signal production of cytokines to stimulate immune cells

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8
Q

What are toll-like receptors?

A

type of pattern recognition receptor (PRR) that recognises molecules shared by pathogens (but distinguishable from host molecules)

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9
Q

Dendritic cells

A

present antigens on surface (trigger adaptive immunity)
present in epithelial tissue
migrate to lymph nodes on activation
numerous dendritic processes branching from cell membranes

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10
Q

Which immune cells are granulocytes?

A

neutrophils
eosinophils
basophils

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11
Q

Eosinophils

A
  • specifically act against multicellular parasites (eg worms) by dissolving cell surfaces
  • involved in IgE-mediated allergic disorders (eg asthma)
  • bilobed nuclei + intracellular granules that stain brick red with eosin
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12
Q

Basophils

A
  • circulating counterparts of tissue mast cells
  • probably involved in inflammation, parasitic infection + allergic reactions
  • important for type 1 hypersensitivity reactions through binding with IgE antibodies
  • bilobed nuclei + large darkly staining intracellular granules
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13
Q

Monocytes

A
  • produced in bone marrow, travel in blood to target tissues + become macrophages
  • large cells, fine ground-glass granules + horseshoe-shaped nuclei
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14
Q

Phagocytosis process

A
  • phagocytes identify pathogens by recognising PAMPs using PRRs (pathogen recognition receptors eg TLRs)
  • pseudopodia extend around pathogen, internalising it
  • engulfed material held in phagosome
  • lysosome fuses with phagosome + releases ROS/enzymes which break down phagosome contents
  • phagocytes present digested protein antigens to cells of adaptive immune system via MHCs on surfaces
  • when phagocyte PRRs are exposed to PAMPs, NFKB is activated (transcription factor that causes release of cytokines + initiation of inflammatory response)
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15
Q

What are the 3 main lymphocyte subtypes?

A

B cells
T cells
Natural Killer cells (NK cells)

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16
Q

B + T cell structure

A
  • small cells
  • round nuclei
  • blue-ish cytoplasm
    (can only be distinguished with specialist serology)
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17
Q

B-cells

A
  • important in humoral/antibody-mediated immunity
  • plasma cells = mature B cells that secrete antibodies which recognise specific foreign antigens + bind to/destroy them
  • memory cells = remember foreign antigen to allow immune system to have quicker antibody response to subsequent infections
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18
Q

T-cells

A

all present CD3 + T-cell receptors (TCR) on surfaces which recognise specific antigens presented in MHC 1/2 molecule

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19
Q

helper T cells (CD4)

A
  • facilitate activation of immune response

- stimulate division + differentiation of effector cells

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20
Q

cytotoxic T cells (CD8)

A
  • provide cell-mediated immunity by targeting + killing infected cells
  • contain granules filled with enzymes (eg perforins)
  • kill tumour cells
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21
Q

regulatory T cells (FOXP3 + CD25)

A
  • AKA suppressor T cells

- limiting immune response to prevent excessive damage to tissues + organs

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22
Q

memory T cells (CD62 + CCR7)

A
  • remember what has happened

- allows immune system to mount faster + more effective response should offending organism return

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23
Q

Natural Killer cells

A
  • larger lymphocyte
  • granules in cytoplasm
  • express CD16 + CD56 (+some express CD8)
  • part of innate + adaptive immune responses
  • can destroy pathogens + infected cells without prior activation by specific antigens
  • particularly important in viral immunity + tumour rejection
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24
Q

Innate immune system features

A
  • first line of defence against any infection
  • very fast
  • non-specific
  • no memory
  • cellular response by innate immune system, chemical response by cytokines + complement, and initiation of acute inflammatory response
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25
Q

What is MHC restriction?

A

MHC prevents immune system from being activated too easily

- ensures T cells can only react to antigen if presented within an MHC complex

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26
Q

How do natural killer cells work?

A
  • do not require activation by specific antigens so can respond immediately
  • self cells protected by inhibitory effects of MHC 1 (expressed on surface of nucleated body cells)
  • cells without MHC 1 likely to be non-self - NK cells release toxic granules - induce apoptosis
  • MHC 1 expression often suppressed if cells infected with viruses or cancerous, therefore NK cells involved in viral immunity + tumour rejection
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27
Q

Describe the 3 pathways that activate the complement system

A

Classical pathway = activated by binding of antigen to IgG/IgM (formation of antigen-antibody complexes)
Alternative pathway = activated directly by microbial components + does not need antigen-antibody components for activation
Mannose-binding lectin pathway = activated by lectin binding to mannose on pathogen surface

28
Q

What do the 3 complement pathways lead to?

A

Formation of C3 convertase enzyme

29
Q

What does C3 convertase enzyme do?

A

bind complement component C3 + split it into C3a + C3b

30
Q

C3a function

A

anaphylatoxin

dissipates to recruit + activate leukocytes

31
Q

C3b function

A
  • binds to + coats pathogens - easier for phagocytes to identify + digest (opsonisation)
  • can bind more C3b to form C5 convertase which binds C5 and splits into C5a (anaphylatoxin) + C5b
32
Q

C5b function

A
  • binds C6, C7, C8 + C9 to form membrane attack complex (MAC)
  • MAC = ring-shaped - tunnels hole in bacterial cell wall allowing water to flood in causing osmotic lysis
33
Q

Complement system functions

A

Formation of anaphylatoxins (C3a, C4a + C5a):

  • cause release of histamine from mast cells
  • C5a - chemotactic + activation agent for neutrophils, monocytes, eosinophils + basophils

Opsonisation:

  • C3b coats walls of microbe
  • neutrophils + macrophages have C3b receptors
Cell lysis (MAC):
- final stage in complement cascade = MAC formation - causes osmotic lysis of cells

Immunoglobulin clearance:
- removal of immune complex from circulation

34
Q

What is a proinflammatory cytokine?

A

small messenger proteins released by immune cells in response to evidence of infection which interact to mediate the acute inflammatory response
(eg interleukins, tumour necrosis factors + chemokines)

35
Q

Main phases of acute inflammation process

A

Vascular phase

Cellular phase

36
Q

Describe the vascular phase of acute inflammation

A
  • Hageman factor activated by collagen contact or contact with microbes
  • clotting system activation
  • complement system activation
  • kinin system activation (bradykinin produced)
  • bradykinin causes vasodilation of arterioles, increased vascular permeability (endothelial cells contract, more space between cells) + pain
37
Q

Describe the cellular phase of acute inflammation

A

predominant cell = neutrophil
- neutrophils attracted to injury site by chemotaxins

Migration of neutrophils:

  • Margination = cells line up against endothelium
  • Rolling = close contact with + roll along endothelium
  • Adhesion = connecting to endothelial wall
  • Transmigration/emigration = cells move through vessel wall to affected area
  • Phagocytosis = once in area, neutrophils phagocytose and destroy pathogen by oxygen-dependent (using ROS), or oxygen-independent (using lysozymes) mechanisms
  • Resolution = neutrophils die by apoptosis + macrophage era begins
38
Q

What are the outcomes of acute inflammation?

A

Resolution + healing = anti-inflammatory cytokines (IL-10+ TGF-beta) produced by macrophages

Continued acute inflammation = IL-8 produced by macrophages recruits more neutrophils

Abscess formation = cytokines + fibrogenic growth factors produced by macrophages

Chronic inflammation = macrophages activate CD4+ helper T-cells

39
Q

Describe the 2 main protective mechanisms preventing the immune system from being activated inappropriately

A

MHC restriction = ensures only antigens presented within context of MHC complexes are able to trigger immune response

Naive T helper cells need second signal from antigen-presenting cells to become fully activated by their specific antigen (dendritic cells provide this using B7 proteins which bind to CD28 receptors on T cell surfaces)

40
Q

What is central tolerance?

A

removal of lymphocytes with receptors specific for self-antigens

41
Q

How is MHC involved in immune tolerance?

A

Thymic medulla cells use MHC to educate T-cells by presenting self-proteins to immature T-cells

  • If immature T-cells have weak binding for for MHC self-peptide they survive (positive selection)
  • If immature T-cells have strong binding for MHC self-peptide they die (negative selection)
  • Some self-reactive T-cells escape thymus. If they are helper T-cells they can help B-cells make antibodies against self
42
Q

What do T helper cells differentiate into?

A

TH1 cells - promote cytotoxic T cells + cell-mediated immunity
TH2 cells - promote B cells + humoral immunity

43
Q

What is humoral immunity?

A

Specific adaptive immune response activated by TH2 cells
Leads to production of B cells + antibodies
Fights extracellular infections

44
Q

Describe the structure of antibodies

A

Y-shaped
2 large heavy chains (structure dictates whether the antibody is IgM, IgG, IgA, IgE or IgD)
2 small light chains
heavy + light chains connected by disulphide bonds
all 4 chains contain constant + variable regions (constant regions always the same, variable regions unique to each B cell + confer antigen specificity)
antigens bend to end of each arm of Y structure
base of antibody binds to complement + phagocytes

45
Q

What are the 5 antibody isotypes?

A

Dictated by structure of heavy chain constant region

IgM, IgG, IgA, IgE, IgD

46
Q

Describe IgM

A

pentameric
expressed on B cell surfaces
produced early in immune response

47
Q

Describe IgG

A

monomeric
provides majority of antibody-based immunity (secondary responses)
opsonisation
found mainly in circulating blood + tissues
crosses placenta to provide passive immunity to fetus

48
Q

Describe IgA

A

dimeric once reaches tissue
found in mucosal areas (GI, respiratory, urinary tracts)
secreted in saliva, tears + breast milk

49
Q

Describe IgE

A

monomeric
binds to allergens + mediates allergic reactions
provides immunity against multicellular organisms (eg parasitic worms)

50
Q

Describe IgD

A

monomeric

signals activation of B cells

51
Q

What is VDJ recombination?

A
  • antibody variable region genes are coded in three parts: V (variable), D (diversity) and J (joining) segments
  • RAG proteins allow B cells to shuffle gene segments around in maturation + recombine them
52
Q

What is isotype class switching?

A

mature B cells activated by specific antigen + produce IgM antibodies + undergo isotype class switching to produce different types of antibody adapted for locations within body

53
Q

How do antibodies fight extracellular infections?

A
  • neutralise toxins by binding to them
  • bind to antigens on pathogen surfaces (agglutinates to impair mobility + opsonises to enhance phagocytosis)
  • antibodies binding to antigens activates classical complement pathway
  • directly activate effector cells (eg dendritic cells, NK cells + cytotoxic T cells)
54
Q

Describe B cell activation

A
  • naive TH0 cells activated by specific antigen = differentiate into TH2 cells
  • TH2 cells locate B cell counterparts by identifying correct antigen within MHC 2 on B cell surface
  • provide B cell with second signal (CD40 ligand which binds to CD40 on B cell surface)
  • release cytokines which promote B cell development (eg IL-2, IL-4 + IL-5)
55
Q

Describe B cell maturation

A
  • B cells mature into plasma cells + begin to make antibodies
  • plasma cells initially produce IgM antibodies
  • isotype class switching produces different types to cover all areas of body
  • clonal expansion of antigen-specific plasma cells
  • antibodies released to tackle infection
56
Q

What is affinity maturation?

A

antibodies with highest affinity for antigen are encouraged to proliferate

57
Q

What happens to plasma cells after infection has been cleared?

A
  • some plasma cells remain as dormant memory B cells
  • only most highly antigen specific B cells produced by affinity maturation will be selected to become memory cells
  • presence of memory cells = immediate plasma cell proliferation + antibody production can occur at time of next infection
  • number of surviving memory cells increases after each reinfection
58
Q

What is cell-mediated immunity?

A

specific adaptive immune response activated by TH1 cells leading to activation of antigen-presenting cells + a cytotoxic T cell response
fights intracellular infections (eg viruses)

59
Q

Describe activation of antigen-presenting cells

A
  • TH1 cell encounters infected antigen-presenting cell + recognises MHC 2 restricted antigen on surface
  • activates APC by providing CD40 ligand second signal + secreting interferon gamma (a cytokine)
  • once activated, APCs increase production of nitric oxide + superoxide radicals - can destroy ingested pathogens more effectively
60
Q

Describe the cytotoxic T cell response

A
  • activated APCs present antigen to specific cytotoxic T cell receptor within an MHC 1 along with a variety of 2nd signals
  • process aided by secretion of IL-2 by TH1 cells + cytotoxic T cells
  • once activated, cytotoxic T cells identify infected cells by recognising antigen within MHC 1 on surface + destroy these cells
61
Q

How do cytotoxic T cells destroy infected cells?

A
  • form immunological synapse (cells touch) + release perforin to make hole in cell wall - release granzymes + granulysin into cell to induce apoptosis + DNA fragmentation
  • FAS ligand interactions between cell surface can induce apoptosis
  • can release interferon gamma which can block intracellular viral replication
62
Q

What happens to cytotoxic T cells once infection has been dealt with?

A
  • most antigen-specific cytotoxic T-cells remain as dormant memory T-cells
  • during reinfection only first signal (MHC + antigen) needed to reactivate cytotoxic T cell (no second signal needed)
  • means any APC (not just dendritic cells) can activate cytotoxic T cells directly (less need for TH1 cell help)
63
Q

Summarise the responses to intracellular + extracellular infections

A 
Intracellular = TH1 = cell-mediated immune response with activated APCs + cytotoxic T cells
Extracellular = TH2 = humoral immune response with B cells + antibodies
64
Q

Tissues/organs of primary immune system

A

(lymphocytes develop + mature)

  • bone marrow
  • thymus gland
65
Q

Tissues/organs of secondary immune system

A

(mature lymphocytes meet pathogens)

- spleen, adenoids, tonsils, appendix, lymph nodes, Peyer’s patches, mucosa-associated lymphoid tissue (MALT)

66
Q

Why do lymph nodes swell in infection?

A
  • more cells than normal enter lymph node

- dendritic cells present antigens to T-cells which help B-cells make antibody

Year 1 (41 decks)

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