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immunology Flashcards

1
Q

What is the difference between innate and acquired immunity?

A
  • innate = rapid first response to infection
  • no immunological memory

Acquired - lag time from exposure to response
(greater than 96 hours)

  • immunological memory, responses are faster and more powerful, basis for protective vaccination against infectious disease
  • specific for each antigen encountered
  • self regulating through regulatory T cells
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2
Q

What are resident immune response cells (innate) and how do they recognise invading pathogens

A
  • phagocytic (eating cells)- macrophages and dendritic cells
  • others - mast cells
  • pathogens - signature molecules (pathogens associated molecular patterns (PAMPS)

Innate immune cells - express partner receptors to these PAMPS called Pattern recognition receptors (PRRs)

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3
Q

Detail some modes of ingestion

A
  • pinocytosis - ingestion of fluid surrounding cells
  • receptor mediated endocytosis - molecules bound to membrane receptors are internalised
  • Phagocytosis - intact particles (bacteria) are internalised whole which is facilitated by ‘opsonisation’
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4
Q

Draw a mental picture of the steps of phagocytosis

A
  • macrophages express a set of PRRs
  • Receptor binding to PAMPs signals the formation of a phagocytic cup
  • cup extends around the target and pinches off, forming a phagosome
  • fusion with lysosomes to form a phagolysosome - killing of pathogens and degradation of contents
  • debris (antigens) is released into extracellular fluid
  • pathogen-derived peptides are expressed on special cell surface receptors (MHC-2 molecules)
    pro inflammatory mediators are released (TNF- alpha)
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5
Q

What is the definition of opsonisation?

A

coating of the pathogen by soluble factors (opsonins) to enhance phagocytosis

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6
Q

When are mast cells initiated? what is their mechanism?

A
  • something that is too large to be engulfed invades (parasite)
  • bind to the pathogen by PRR - PAMP - (degranulation - release of pre-formed pro-inflammatory substances (histamines))
  • gene expression - production of new pro-inflammatory substances (leukotrienes and prostaglandins)
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7
Q

What leads to local, acute inflammation?

A

release of pro-inflammatory mediators - NO, prostaglandins histamines etc

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8
Q

How does inflammation affect healthy tissues?

A
  • vascular changes
  • recruitment and activation of neutrophils (transendothelial migration)
  • chemicals are produced that attract neutrophils to the site of infection
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9
Q

What are the steps of transendothelial migration?

A

1 - margination of neutrophils to the endothelium near sites of damage

2 - binding of neutrophils to adhesion molecules on endothelial cells

3 - migration of neutrophils across endothelium via process of diapedesis

4 - movement of neutrophils within the tissues by chemotaxis

5 - activation of neutrophil by PAMPs and TNFalpha

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10
Q

What are the three jobs of neutrophils?

A

phagocytosis - use PRR to bind and phagocytose, killed using two mechanisms (phagolysosomal killing and Reactive oxygen species)

  • degranulation - release of antibacterial proteins from neutrophil granules directly into extracellular environment can also cause tissue damage and systemic inflammation
  • Neutrophil extracellular traps
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11
Q

How does reactive oxygen species work?

A
  • NADPH oxygenase-dependant mechanism (repiratory burst) produces ROS
    1 - neutrophil activation
    2- assembly of the NADPH oxidase complex
    3 - production and release of ROS into phagolysosome
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12
Q

How is the acute phase response driven?

A
  • pro inflammatory mediators released by activated macrophages
  • mediated by proteins secreted in the liver such as C3 and MBL (complement) and C reactive protein - primes bacteria for destruction by complement system)
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13
Q

How is a virus dealt with by the immune system?

A
  • release cytokines called interferons which:
  • signal neighbouring unaffected cells to destroy RNA and reduce protein synthesis
  • signal neighbouring infected cells to undergo apoptosis
  • activated immune cells such as natural killer cells - recognise and destroy virally-infected cells (and cancer cells)
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14
Q

What is the purpose of the complement system?

A
  • opsonisation
  • direct pathogen killing
  • acute inflammation
  • leukocyte recruitment§
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15
Q

Describe what the different pathways of the complement system to cleave C3?

A

Classical pathway, mannose binding lectin pathway and the alternative pathway

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16
Q

How does the mannose-binding lectin pathway work? - how does it lead to downstream complement pathway?

A
  • MBL binds to manose on bacterium to activate C3 convertase to cleave into C3b and C3a - c3b turns into an alternative pathway to convert C3
  • C3b then binds to pathogen surface and cleaves C5 into C5b and C5a - membrane attack complex is activated by C5b
  • C3b is also involved in opsonisation
  • C3a and C5a is used for acute inflammation
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17
Q

Why are dendritic cells so important?

A

bridge the gap between the innate immune response and acquired immune system responses

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18
Q

What are B and T cells involved in?

A

B cells - antibodies that attack pathogens circulating in the blood and lymph

key role in defence against extracellular pathogens

T cells - cellular immune response - defence against intracellular pathogens

CD4+ T cells - regulators of the entire immune system

CD8 T cells - kill infected body cells

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19
Q

How do B and T cells recognise pathogens?

A

pathogens have different antigens that are recognised by individual T and B cells

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20
Q

What type of cell is a B cell? what is its structure?

A
  • it is an antibody
  • complex of four polypeptide chains - 2 light chains and 2 heavy chains
  • each antibody has a unique variable region that binds to 1 specific antigen
  • can either be membrane bound or soluble
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21
Q

How does a T cell work?

A
  • only recognise peptide antigens

- can express thousands of copies of a single antigen receptor

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22
Q

What condition must be filled in order for a T cell to recognise a peptide

A

can only recognise peptide antigens presented to their TCRs by MHC molecules

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23
Q

What is the function of Major histocompatibility complex?

A

display peptide antigens to T cells ( many different peptides to T cells)

24
Q

What is the difference between class 1 and class 2?

A

class 1 - on nucleated cells, present peptide antigens to CD8+ T cells

class 2 - only on dendritic cells, macrophages and B cells

present peptide antigens to CD4+ T cells

25
Q

where do T cells and B cells develop in the body?

A

primary lymphoid tissue - bone marrow or spleen

26
Q

where do B cells encounter antigens?

A
  • B cell zone in secondary lymphoid tissues

- soluble antigens and opsonised antigens are transported in lymph to the B cell zone in the lymph zone

27
Q

Where do T cells encounter antigens?

A

1 - dendritic cells phagocytose pathogen derived particles and antigens
2 - pro-inflammatory TNFa stimulates immature tissue resident dendritic cells to increase expression of co-stimulatory molecules
3 - dendritic cells digest ingested proteins and display small peptides derived from these on their cell surface
in the T cell zone in the lymphoid tissue

28
Q

How do B cells become fully activated?

A
  • signal 1 - BCR and antigen
  • Signal 2 help from T helper cells
  • they then differentiate into plasma cells, into antigen specific antibodies and then can battle pathogens
29
Q

What is initially secreted by short lived plasma cells?

A

What is initially secreted by short lived plasma cells?

30
Q

What is produced after the short lived plasma cells?

A
  • B cells mutate so they change into low to high affinity antibodies
  • switch the class of antibody they produce
    then differentiate into long lived plasma cells and long lived memory B cells
31
Q

How does an antibody kill and eliminate pathogens?

A
  • recognition - binding to antigen,

- effector - clearance mechanisms of the heavy chain (Fc region) with effector molecules, complement and Fc receptors

32
Q

what does an IgM molecule look like when its membrane bound and in its secreted form?

A

membrane bound - monomeric form, IgM serves as the B cell antigen receptor

secreted - pentameric form is the first!!! Ig types produced during humeral response

33
Q

What is the definition of agglutination? what is it mediated by?

A
  • the action of an antibody cross linking multiple antigens producing clumps of antigens
  • increases efficacy of phagocytosis and prevents viruses from binding to and infecting host cells
  • mediated by IgM and IgG
34
Q

What is the most common type of antibody? detail some functions

A
  • most common type of antibody is IgG and is monomeric form when secreted

agglutination, foetal immune protection, neutralisation (best with IgG and IgA), opsonisation and natural killer cell activation

35
Q

What is the function of IgD?

A
  • membrane bound monomeric form - IgD serves as a B cell antigen receptor - mediates B cell activation
    not well understood
36
Q

What is IgA good for?

A

most common in the body

  • monomeric form and it is involved in neutralisation
  • neonatal defence - transported into colostrum and in breast milk to protect the GI tract of neonates(dimeric form)
37
Q

What is IgE involved with?

A
  • trigger allergic response
  • least abundant type of Ig
  • provides immunity to parasites such as helminths
38
Q

What happens after T cells come into contact with the pathogen in the secondary lymphoid tissue

A

become active cells,

entry into cell cycle and clonaly expand then differentiate into effector cells and then memory cells

39
Q

What are cellular immune responses mediated by?

A
  • CD4+ T cells
  • naive CD4 T cells proliferates into
  • CD4+ Th0 cells
  • which differntiate again into CD4 effector TH cells
    (Th1, Th2, Tfh and regulatory T cells)
40
Q

What do Th1 cells do?

A

Create a super activated macrophage and release pro-inflammatory signals

41
Q

How can some pathogens evade phagolysosomal killing?

A

killing macrophages - infect and propagate in macrophage (legionella, mycobacteria)

42
Q

What do T folicular helper cells fo?

A

They play a critical role in protective immunity helping B cells produce antibody against foreign pathogens.

43
Q

What do antigen activated CD8+ cells proliferate and differentiate into?

A

killer cells - cytotoxic lymphocytes

migrate out of lymph and enter sites of infection in order to kills host cells

44
Q

How do cytotoxic T cells work?

A

recognise and bind virus-infected cell
CTL programmes target for death inducing DNA fragmentation
CTL migrates to new target
Target cell dies by apoptosis

45
Q

When are IL-2 released?

A

first part of the adaptive response (Th0),

46
Q

What is involved in the innate immune response

A

Mast cells, natural killer cells, phagocytes and complement

- responsible for acute inflammation and killing of pathogens

47
Q

What is pus?

A

Dead and dying neutrophils + tissue cells + microbial debris

48
Q

When are cytokines produced?

A

response to infection, inflammation or tissue damage

49
Q

What are the local effects of inflammation?

A

Redness, heat, swelling, pain and loss of function

50
Q

What does the liver release in response to pro-inflammatory cytokines?

A

Acute phase proteins - IL1 and IL6, TNF - infection, trauma, chronic nflammation

51
Q

Why are C3a and C5a important in immunology?

A

bind onto mast cells and basophils and release granules producing histamine and chemokines

52
Q

How do T and B cells recognise pathogens?

A

T cell antigen receptor = membrane bound protein heterodimer
Alpha and Beta chain

B cell antigen receptor = membrane bound antibody (IgM or IgD)
has light and heavy chain disulphide bridges

53
Q

How do B cells switch their class?

A

Changing their antibody heavy chain segment

54
Q

What are some important facts surrounding IgG

A

Most abundant immunoglobulin in blood serum, most dominant in the memory immune response and is transferred across the placenta into the foetal circulation

55
Q

What is important in the activation of

the complement system via the classical pathway?

A

IgG

IgM is also relevant for the classical pathway.

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