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Phase 3 > Week 0 > Flashcards

Week 0 Flashcards

1
Q

What are the 2 categories of innate immunity?

A

Soluble factors and cellular factors

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2
Q

What are the types of soluble factors?

A

antibacterial factors and complement system

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3
Q

What are the cellular factors of innate immunity?

A

scavenger phagocytes

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4
Q

What are the main types of antibacterial factors?

A

lysozyme and lactoferrin

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5
Q

Describe lysozyme

A

enzymes at mucosal surfaces

Active in breaking down the gram positive cell wall

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6
Q

Describe lactoferin

A

Protein found at mucosal surfaces
Chelates iron and therefore reduces soluble iron in the GI / respiratory ttract
Inhibits the growth of bacteria

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7
Q

What are the 3 types of complement pathways?

A

Classical
MB-lectin
Alternative

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8
Q

Describe the classical pathway

A

antigen:antibody complexes

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9
Q

Describe the MB-lectin pathway

A

lectin binding to pathogen surfaces

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10
Q

Describe the alternate pathway

A

pathogen surfaces

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11
Q

What does the activation of complement lead to?

A

Recruitment of inflammatory cells
Opsonisation of pathogens
Killing of pathogens

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12
Q

What is c3a involved in?

A

Inflammation

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13
Q

What is c3b involved in?

A

opsonisation and phagocytosis

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14
Q

What is c5a involved in?

A

Late inflammation

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15
Q

What are the major functions of macrophages?

A

Phagocytosis
Antigen presentation
Cytokine production

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16
Q

What are macrophages differentiated from?

A

Monocytes

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17
Q

Describe pattern recognition receptors

A

recognise molecules found commonly in micro-organisms.
Able to recognise extracellular and intracellular threats
Respond to bacteria, fungi and yeast

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18
Q

What are the main actions of neutrophils?

A

Chemotaxis
Phagocytic
Degranulate
Die locally

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19
Q

Describe neutrophils

A

The foot solider of the immune system
50-70% of WBCs
provide a rapid response to infection

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20
Q

Describe eosinophils

A

Classically respond to parasites

pathological role in allergy

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21
Q

What are the main roles of eosinophils?

A

chemotaxis
degranulation
cytokine production

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22
Q

Describe Basophils /mast cells

A

mast cells are the border guard of the immune system, guarding mucosal sites
important role in allergy

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23
Q

What are the main roles of basophils / mast cells?

A

degranulation

cytokine release

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24
Q

Describe dendritic cells

A

derived from the same precursor as macrophages

Prototype antigen presenting cell

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25
Q

What are the main roles of dendritic cells?

A

phagocytosis
migration
antigen presentation

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26
Q

What are the two types of adaptive immunity?

A

humoral and cellular

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27
Q

Describe the humoral response

A

B cells
antibodies
extracellular pathogens

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28
Q

Describe the cellular adaptive response

A

CD4 T cells and CD8 T cells

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29
Q

What are the actions of antibodies?

A

opsonise for phagocytose
activate complement for lysis
neutralise toxins and pathogen binding sites

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30
Q

Where do antibodies differ?

A

In Fc regions

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31
Q

Describe IgM

A

Main antibody of primary immune response
low affinity
activates complement

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32
Q

Describe IgG

A

Main antibody of secondary immune response
Higher affinity as part of secondary response
Activates complement, Binds Fcy receptors of phagocytes, crosses placenta

33
Q

Describe IgA

A

Antiseptic paint
present in secretions and lines epithelial surfaces.
neutralises by blocking binding of pathogens

34
Q

Describe IgE

A

High affinity binding to mast cells

Role in allergy

35
Q

Describe the primary antibody response

A

usually 5-10 days
Smaller
Usually more IgM>IgG
lower average affinity, more variable

36
Q

Describe the secondary antibody response

A

usually 1-3 days
larger
Relative increase in IgG and under certain situations, in IgA or IgE (heavy chain isotope switching)
Higher average affinity

37
Q

How do T cells help B cells?

A 
Clonal expansion of specific B cells
Progression to antibody secreting cells 
progression to memory B cells
Isotope switching to IgG, IgA and IgE
affinity maturation
38
Q

Describe T cell receptors

A

on the surface of T cells and only recognises antigen when it is presented in a MHC molecule
Recognises short peptide lengths

39
Q

How do B cells develop to prevent autoimmunity?

A

develop in bone marrow

if receptor binds strongly to self antigen in bone marrow it dies by apoptosis

40
Q

How do T cells develop to prevent autoimmunity?

A

originate in bone marrow and migrate to thymus

if binds strongly to self antigen in thymus it dies by apoptosis

41
Q

What is meant by the second signal, involved in preventing autoimmunity?

A

activation of lymphocytes requires presence of danger signals to activate. if antibody/TCR engaged in absence of “second signal” then cell likely to become anergic

42
Q

Describe class 1 MHC

A

presents to CD8 T cells
found on all nucleated cells
Presents intra-cellular antigen

43
Q

Describe class II MHC

A

presents to CD4T cells
Presents extra-cellular derived antigen
Found on APCs, macrophages and B cells

44
Q

Describe Th1 cells

A

IFN gamma secretion

host defence against intracellular microbes, inflammation

45
Q

Describe Th2 cells

A

IL-4, IL5, IL13 secretion

host defence against helminths; allergic reactions

46
Q

Describe Th17 cells

A

IL17 secretion; host defence against some bacteria; inflammatory disorders

47
Q

Describe T regulatory cells

A

Act to regulate function of other immune cells

48
Q

What are the primary organs of the adaptive immune system?

A

Thymus and bone marrow

49
Q

What are the secondary organs of the adaptive immune system?

A

lymph nodes
spleen
Mucosal associated lymphoid tissue of GI tract and bronchial tracts

50
Q

Give an overview of the adaptive immune system

A

provides specific antibodies to the innate immune system to enhance pathogen clearance
Provides cytokines to the innate immune system to upregulate activity
Finishes off the job of clearing pathogens
Develops a memory to prevent future infection

51
Q

Describe the secondary response

A

Memory B cells and memory T cells already present at a high frequency
Memory lymphocytes have lower threshold for activation and actively patrol the sites of previous pathogen entry
Preformed antigen specific IgA prevents pathogen binding
Preformed high affinity IgG rapidly opsonises pathogen for phagocytosis

52
Q

How many types of hypersensitivity are there?

A

4/5

53
Q

Describe type I hypersensitivity

A

immediate, atopic

IgE mediated

54
Q

Describe type II hypersensitivity

A

cytoxic, antibody dependent

IgM or IgG bound to cell / matrix Ag

55
Q

Describe type III hypersensitivity

A

Immune complex

IgM or IgG bound to soluble Ag

56
Q

Describe type IV hypersensitivity

A

T cells (CD4+ and CD8+)

57
Q

Describe type V hypersensitivity

A

Receptor mediated

IgM or IgG bound to receptor (i.e Grave’s disease)

58
Q

What are the specific characteristics of type I hypersensitivity?

A

Response to challenge occurs immediately
Tends to increase in severity with repeated challenge
Predominantly mediated by IgE bound to mast cells

59
Q

Give examples of type I hypersensitivity

A

Asthma
Eczema
Hay fever

60
Q

Describe the steps involved in allergy

A

Sensitisation
Mast cells primed with IgE
Re-exposure to antigen
Antigen binds to IgE assoiciated mast cells
Mast cells degranulate releasing; toxins, tryptase, cytokines. chemokines, prostaglandins, leukotrienes
Pro-inflammatory process stimulates and amplifies future responses

61
Q

Describe the early tissue effects in allergy

A

occurs within minutes of exposure to antigen exposure
Occurs largely as a result of histamine and prostaglandins - smooth muscle contraction and increased vascular permeability

62
Q

Describe the late phase tissue effects in allergy

A

hours to days after exposure
Principally mediated through recruitment of t Cells and other immune cells to site
Results in; sustained smooth muscle contraction/hypertrophy, tissue remodelling

63
Q

Describe anaphylaxis

A

Severe, systemic type I hypersensitivity
Widespread mast cell degranulation caused by systemic exposure to antigen (e.g. penicillin)
Vascular permeability is principle immediate danger; soft tissue swelling threatening airway. loss of circulatory volume causing shock

64
Q

What is meant by type II hypersensitivity

A

caused by binding of antibodies directed against human cells
IgG usual cause
Uncommon cause of allergy (drug associated haemolysis)
Common cause of autoimmune disease

65
Q

Give an example of an illness caused by type II hypersensitivity

A

Bullous pemphigoid

66
Q

Describe the steps involved in type II (V) hypersensitivty

A

sensitisation
Opsonisation of cells
Cytotoxicity - complement activation, inflammation, tissue destruction

67
Q

Describe the specific step involved in type V hypersenstivity

A

direct biological activation with antigen (i.e receptor activation, impaired enzyme action)
Graves disease

68
Q

Give a description of type III hypersensitivity

A

Mediated by immune complexes bound to soluble antigen
Cause of autoimmune disease and drug allergy
Aggregates in small blood vessels _ direct occlusion, complement activation, perivascular inflammation

69
Q

Give a description of type IV hypersenstivity

A

also known as delayed type hypersensitivity
presents several days after exposure
mediated by the action of lymphocytes infiltrating area

70
Q

What is autoimmune disease?

A

harmful inflammatory response directed against “self” tissue by the adaptive immune response - organ specific or systemic

71
Q

Describe myasthenia Gravis

A

syndrome of fatiguable muscle weakness - limbs, respiratory, head and neck
Caused by IgG against acetylcholine receptor
Antibody blocks receptor and prevents signal transduction

72
Q

Give examples of systemic autoimmune diseases

A

Rheumatoid arthritis
systemic lupus erythematosus
inflammatory bowel disease
systemic vasculitis

73
Q

What are the systemic effects of RA?

A 
pulmonary nodules and fibrosis
Percarditis and valvular inflammation
small vessel vasculitis
soft tissue nodules 
skin inflammation
weight loss
anaemia
74
Q

Describe rheumatoid factor

A

IgM and IgA directed against IgG Fc region
Forms large immune complexes; high concentration within synovial fluid
Also found in other tissues

75
Q

Describe the general pathophysiology of RA

A

inflammation leads to release of PAS from inflammatory cells
Alters variety of proteins by converting alanine to citrulline
In RA, anti-citrullinated protein/peptide antibodies are common

76
Q

Describe the pathophysiology of RA in the joints

A

Amplification of inflammatory cascade
Further chemoattraction of inflammoty cells into synovial; macrophages, neutrophils, lymphocytes
Osteoclast activation and joint destruction
Fibroblast activation and synovial hyperplasia
Systemic inflammation

77
Q

Describe the pathogenesis of autoimmune disease

A

genetic predisposition
environmental factors
Recognition of self antigens by the immune system as foreign
Persistence of inflammatory response to develop chronic of disease

78
Q

What are the environmental factors associated with autoimmune disease?

A

infection
geographical factos
modifiable personal risk factors

Phase 3 (15 decks)

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