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2A content- Sameera > 2. IMMUNOLOGY > Flashcards

2. IMMUNOLOGY Flashcards

1
Q

purpose of immune system

A

discriminate self from non-self

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2
Q

what r the 2 types of non specific defence mechanisms and give 2 examples for each

A

physical: skin, cilia
chemical: sweat, tears

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3
Q

What r the two components of a general immune response

A

inflammation and complement

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4
Q

where r complements produced and where can they be found when inactivated

A

liver
circulate in blood

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5
Q

what r the 2 functions of a complement

A

marks pathogens for destruction
clumps together lots of antigens

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6
Q

what is the function of inflammation (2 things- steps, same point)

A

increase blood flow to an area
this brings immune cells to the site of infection

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7
Q

name the three types of lymphoid organs

A

primary, secondary, tertiary

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8
Q

what happens at primary lymphoid organs (general)

A

where leukocytes r synthesised

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9
Q

what happens at secondary lymphoid organs (general) and what does this mean for naive cells

A

leukocytes monitor areas which allows naive cells to interact with antigens

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10
Q

what r tertiary lymphoid organs, where do they form and in response to what

A

collections of immune cells that form in non-lymphoid tissues in response to local chronic inflammation

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11
Q

what r the two primary lymphoid organs

A

bone marrow and thymus

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12
Q

what is the bone marrow the site of (2)

A

site of immune cell synthesis and site of B cell maturation

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13
Q

what is the thymus the site of

A

site of t cell maturation

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14
Q

name the secondary lymphoid organs (3)

A

lymph nodes, spleen and mucosal associated lymphoid tissues (MALT)

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15
Q

example of MALT

A

eg Peyer’s Patches in the small intestines

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16
Q

what do secondary lymphoid organs involve the formation of

A

germinal centres

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17
Q

what two cells do germinal centres produce (2)

A

produces long-lived antibody secreting plasma cells and memory B cells

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18
Q

what are the lymph nodes the site of (1)

A

site of dendritic cell, B and T cell interactions

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19
Q

what is the spleen the site of removal of (2)

A

site of removal of RBCs and antibody coated bacteria

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20
Q

where r B cells found in lymph nodes

A

lymphoid follicles in cortex

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21
Q

where r T cells found in lymph nodes

A

paracortex

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22
Q

what cell does a dendritic cell interact with in the lymphatics and how do they enter and what with

A

interact with naive CD4+ cells to active them in the paracortex
enter with antigen in afferent lymphatics

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23
Q

what happens to activated B and T cells in lymphatics (2)

A

T cell differentiate into effector or memory cells
B/T cells exit via lymphatics

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24
Q

what is the general structure of the spleen

A

red and white pulp

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25
Q

function of red pulp

A

mechanically filtrates the RBCs

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26
Q

function of white pulp (1)

A

activates humoral and cell mediated immune response

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27
Q

what type of immune response is humoral immunity (1) and what does it involve (2) and what for (1)

A

adaptive immune response
involves B cells and antibodies for extracellular pathogens

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28
Q

what type of immune response is cell mediated immunity, (1) what does it involve (1) and what for (1)

A

adaptive immune response
involves mature T cells for intracellular pathogens

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29
Q

Why is the adaptive system required? (2)

A
  1. innate immunity can be evaded
  2. memory for faster response to same antigen
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30
Q

what r germinal centres rich in

A

B cells

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31
Q

what r PALS rich in and what does it stand for

A

(periarteriolar lymphoid sheath) r rich in T cells

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32
Q

when r tertiary lymphoid organs present and give an example (1)

A

present pathologically due to chronic inflammation eg primary chronic infection

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33
Q

what two lymphoid organs have germinal centres

A

secondary and tertiary

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34
Q

define Haematopoiesis

A

production of all the cellular components of blood and blood plasma

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35
Q

recall Haematopoiesis pathways

A

find picture

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36
Q

compare receptors for innate and adaptive immunity and give 2 examples for adaptive

A

innate= broad
adaptive= highly specific (b and t cell receptors)

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37
Q

compare onset for innate and adaptive immunity

A

innate= fast
adaptive= slow

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38
Q

compare amplification for innate and adaptive immunity

A

innate= no
adaptive= yes

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39
Q

compare duration for innate and adaptive immunity

A

innate= short
adaptive= long

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40
Q

compare self discrimination for innate and adaptive immunity

A

innate= not as good
adaptive= good

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41
Q

compare memory for innate and adaptive immunity

A

innate= none
adaptive= yes

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42
Q

compare regulation for innate and adaptive immunity

A

innate= not as controlled
adaptive= highly regulated

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43
Q

what two things can innate cells recognise and with what?

A

PAMPs and DAMPs
with PRRs

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44
Q

what does PAMPs and DAMPs and PRRs stand for

A

pathogen/damage associated molecular pattern
pattern recognition receptors

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45
Q

what r the two types of PRRs

A

membrane bound PPRs and cytoplasmic (free) PRRs

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46
Q

example of membrane bound PRR (2)

A

Toll like receptors and C-type lectin receptors

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47
Q

example of cytoplasmic bound PRR (1)

A

NOD-like receptor

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48
Q

define pattern recognition receptors, what is their origin and how is their conservation

A

receptors from germline with a great degree of evolutionary conservation

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49
Q

which TLRs r intracellular and what do they detect

A

TLR 3, 7, 8, 9
detect nucleic acids from intracellular pathogens (viruses and bacteria)

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50
Q

what TLRs r extracellular

A

all except 3, 7, 8, 9

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51
Q

How do TLRs work (4 steps)

A
  1. binds to PAMP
  2. secondary messengers generated in cell
  3. secretion of inflammatory mediators (IL1,12, TNFa)
  4. this stimulates activity of innate immune cells
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52
Q

what cells r TLRs found on

A

macrophages, dendritic cells and neutrophils (all APCs)

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53
Q

what is the PAMP TLR 2 recognises and where is this PAMP present

A

lipoteichoic acid
gram + bacteria and mycobacteria eg TB

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54
Q

what is the PAMP TLR 3 recognises and where is this PAMP present

A

double stranded RNA of viruses

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55
Q

what is the PAMP TLR 4 recognises and where is this PAMP present

A

lipopolysaccharide on gram - bacteria, viruses

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56
Q

what is the PAMP TLR 5 recognises and where is this PAMP present

A

flagellin on flagellated bacteria

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57
Q

what is the PAMP TLR 7/8 recognises and where is this PAMP present

A

single stranded RNA on viruses, bacteria

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58
Q

what is the PAMP TLR 9 recognises and where is this PAMP present

A

double stranded unmethylated DNA on viruses, bacteria and protozoa

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59
Q

what is significant about TLR 10

A

only present in humans

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60
Q

name the 7 innate cells (think TELEMANN)

A

dendritic cells
macrophages
neutrophils
basophil
eosinophil
mast cells
NK cells

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61
Q

why r dendritic cells important for immune responses

A

connects the innate and adaptive immune responses

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62
Q

origin of dendritic cells

A

mesenchymal origin

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63
Q

where can dendritic cells be found generally

A

in tissue that has contact with outside environment: skin, nasal lining, stomach and intestines

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64
Q

main dendritic cell and location (2)

A

interstitial dendritic cells (present in bone marrow and blood)

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65
Q

4 functions of dendritic cells

A

phagocytic, antigen presenting, cross presentation, cytokine production

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66
Q

What is cross presentation and explain dendritic cell cross presentation

A

Presentation of exogenous antigens via MHC by a APC
Dendritic cells present exogenous antigens in the context of MHC II to activate T cytotoxic cells

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67
Q

what 3 things can dendritic cells recognise

A

cytokines, PAMPS and DAMPs

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68
Q

characteristics of mature dendritic cells (5)

A

increased MHC II expression
increased secretion of pro-inflammatory cytokines
decreased phagocytic capacity
increased CCR7 expression
increased glycolysis

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69
Q

what is CCR7

A

chemokine receptor that guides DCs to secondary lymphoid organs

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70
Q

3 functions of macrophages

A

phagocytosis, antigen presentation and cytokine secretion

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71
Q

appearance of macrophage nucleus (3) and what do its lysosomes contain (1)

A

round single nucleus often with a small indentation
peroxidase

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72
Q

where r macrophages derived from (2)

A

blood monocytes or as tissue resident macrophages

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73
Q

where r tissue resident macrophages derived from and how do they persist

A

derived from yolk sac/ foetal liver during development
persist in tissues via self renewal

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74
Q

what r the identifiers of macrophages (2)

A

CD14+ and CD 40+

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75
Q

3 principle cells of chronic inflammation

A

macrophages, plasma cells, lymphocytes (T and B)

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76
Q

what r macrophages activated by (1)

A

INF gamma (IT IS i NOT t)

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77
Q

what can macrophages produce and give 3 examples

A

cytokines: TNF-alpha, IL-1 and IL-12

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78
Q

what is TNF alpha

A

a pro-inflammatory molecule

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79
Q

what is opsonisation and what two things can bind?

A

marking for phagocytosis by antibody and complement

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80
Q

explain the steps of opsonisation for antibodies

A
  1. antibody binds to pathogen via their Fab region
  2. macrophages have Fc receptors that bind to the antibody
  3. this allows for phagocytosis of the bacteria that the antibody has bound to
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81
Q

explain steps of opsonisation for complement

A

1.antibody binds to pathogen via their Fab region
2. complement binds to antibody Fc region to form a complex
3. macrophages have complement receptors that recognise this complex which is then phagocytose

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82
Q

what is the most abundant leukocyte and what %

A

neutrophils 70

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83
Q

what do neutrophils secrete to kill pathogens

A

secretes superoxides which r toxic

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84
Q

What r the contents of neutrophils (2)

A

have 2 main intracellular granules: primary and secondary lysosomes

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85
Q

what 2 types of infections r neutrophils raised in

A

bacterial, bacterial pyogenic infections

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86
Q

two methods neutrophils use to kill pathogens

A

respiratory burst and phagocytosis

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87
Q

what is the principle cell of acute inflammation

A

neutrophils

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88
Q

what chemokine attracts neutrophils to site of infections and what two functions does this have

A

IL 8- role in neutrophil production and recruitment

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89
Q

example of polymorphonucleur cells and where can these be found

A

Barr body: present in female neutrophils

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90
Q

what is the GENERAL lifespan of neutrophils (gist)

A

short life

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91
Q

explain the steps of neutrophils movement in acute inflammation

A
  1. neutrophils attracted by IL 8
  2. E-selectin (adhesion molecule) on capillary endothelium is activated by IL-1 and TNF-alpha from damaged cells and binds to the CD15 glycoprotein on neutrophils in blood
  3. neutrophils slow down and roll along endothelium lining
  4. ICAM-1 on endothelium binds to intern on neutrophil, causing it to stop
  5. diapedesis: neutrophil squeezes through the endothelium (holes made by C3a, C5a, chemokine, histamines and prostaglandins)
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92
Q

location of immature and mature basophils

A

immature= bone marrow
mature= circulating in blood

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93
Q

what activates basophils

A

IgE cross linking with its affinity IgE-Fc receptors (Fcε)

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94
Q

what three substances do basophils secrete

A

histamine, serotonin and heparin

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95
Q

what medical condition is basophils important in and give 4 examples

A

hypersensitivity reactions
hay fever, anaphylaxis, asthma, tropic dermatitis

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96
Q

where can basophils not go and what cells do this instead?

A

egress into tissues, mast cells

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97
Q

what 1 type of infection do eosinophils deal with

A

parasitic

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98
Q

what do eosinophils secrete and give three examples

A

release cationic granules eg major basic protein, ROS and eicosanoids

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99
Q

alternative name for granulocytes

A

polymorphonucleur cells

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100
Q

three granulocytes (BEN acronym)

A

basophil, eosinophil, neutrophil

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101
Q

what r the 3 main professional phagocytes

A

neutrophils, macrophages, dendritic cells

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102
Q

what type of killing mechanism is used in phagocytosis

A

oxygen dependant mechanism

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103
Q

what does a combined phagosome and lysosome form

A

phagolysosome

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104
Q

what two substances r released phagolysosomes to kill pathogens and what condition is maintained and why this condition

A

granzyme B and azurophillic granules and a low pH to ensure optimum conditions for destruction of pathogens

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105
Q

what is the MAIN oxygen dependant mechanism for killing

A

respiratory burst

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106
Q

explain the 5 steps of resp burst

A
  1. electrons pumped into phagolysosome by NOX 2
  2. electrons combine with molecular oxygen to make a superoxide
  3. hydrogen and chloride ions are co-transported in
  4. H+ combined with superoxide to make peroxide
  5. peroxide combines with chloride ions to make HOCL (catalysed by MPO) which is bactericidal
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107
Q

what two reactions r mast cells present in

A

parasitic infection and allergic reactions

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108
Q

at what surfaces can mast cells be found

A

at mucosal surfaces

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109
Q

what is essential for massst cell development

A

stem cell factor

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110
Q

what r mast cells activated by

A

IgE binds to allergen then mast cell is activated via Rc receptor 1 (immune complex formed with IgE crosslinking Fcε R1)

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111
Q

what do mast cells secrete when they degranulate (5)

A

histamine, TNF alpha, IL 4 and 13 and lipid mediators
happy technicians found 13 lipid mediators

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112
Q

what does histamine do (2)

A

increase vascular permeability
smooth muscle contraction

113
Q

what does IL 4 and 13 promote (2 things- be careful)

A

promotes Th2 differentiation
promotes IgE production

114
Q

what does TNF alpha do (1)

A

promotes tissues inflammation

115
Q

what do the lipid mediators prostaglandin and leukotrienes do (4)

A

increases vascular permeability
smooth muscle contraction
stimulates mucus secretion
chemoattractants for immune cells

116
Q

where can NK cells travel (2)

A

blood and tissues

117
Q

marker for NK cells (1)

A

CD 16+

118
Q

what is the unique killing mechanism for NK cells

A

antibody-antigen dependant cellular cytotoxicity (ADCC)

119
Q

how do NK cells recognise self and non-self

A

recognise self and non-self by the presence of MHC I on cell surfaces

120
Q

what cells do NK cells activate, what do these do and how

A

cytotoxic T cells- which then act on tumor cells
NK cell cytokine production

121
Q

explain the 3 steps of ADCC

A
  1. IgG binds to surface antigens on the pathogen-infected or cancer cells
  2. NK cells have Fc receptors (CD 16) that recognise that antibody Fc region
  3. this cross linking triggers degranulation of granules that contain perforin and granzymes that induce apoptosis and cell death
122
Q

how r virally infected cell identified by NK CELLS (2 step answer)

A

viral proteins expressed on the surface of cells during viral replication become antibody targets. Antibodies bind to this and NK cells can recognise the Fc region of the antibodies

123
Q

how r cancer cells identified by NK cells

A

cancers down regulate MHC I mediated antigen presentation so when NK cell receptors detect low levels of MHC I on cell surfaces, they become activated and try to kill the cancer cill

124
Q

what r the three main APCs and what do they all present in the context of what

A

macrophages, B cells and dendritic cells
all present exogenous antigens in the contact of MHC II

125
Q

what is the most effective/ potent APC

A

dendritic cells

126
Q

where do dendritic cells egress to

A

egress to secondary lymphoid organs

127
Q

which cells can present MHC I

A

all nucleated cells (so not RBCs)

128
Q

what does MHC stand for, what is it and what is its major role

A

major histocompatability complex
cell surface glycoprotein
presents antigens to T cells

129
Q

where r MHCs coded for

A

chromosome 6

130
Q

where are exogenous antigens processed in the cell and presented in which context

A

exogenous antigens are processed in the endoplasmic reticulum and are presented in context of MHC II

131
Q

where r endogenous antigens processed and presented by

A

endogenous antigens r processed in endolysosomal compartment and are presented in context of MHC I

132
Q

what forms an immune synapse (2)

A

a APC bound to a T cell

133
Q

what three things do immune synapses require to be successful for a response to be generated

A
  1. primary receptor binding eg TLR to MHC II
  2. co-stimulatory molecules binding (co-receptors interacting on the bound DC and T cell in number 1)
  3. appropriate cytokines being released
134
Q

what happens to a T cell on initial encounter with a new antigen

A

T cells will differentiate into memory or effector T cells

135
Q

what r the two adaptive immune cells

A

B and T cells

136
Q

what is the identifying T cell marker and what is its function

A

CD 3- starts intracellular signalling which activates the T cell

137
Q

can T cells express CD 4 and 8 and what happens to this ability after thymic education

A

can express both but thymic education leads to only 4 or 8 being retained not both

138
Q

what r the three generic types of T cells

A

naive, effector or memory

139
Q

what is a naive T cell

A

not encountered any antigens before

140
Q

what is the T cell marker of activation

A

CD 25

141
Q

what is memory and naive T cell identifier

A

memory= CD 45RO+
naive= CD45RA+

142
Q

how do T cells recognise antigens and what is the exception to this

A

MHC binds to T cell receptors
exception= superantigens

143
Q

what 4 things can (effector) T cells differentiate into after activation and what 2 factors does this depend on

A

T helper cells (1, 2, 9)
TfH (follicular helper cells)
depends on transcription factors and cytokine stimulation

144
Q

what cell induces apoptosis in virally and cancer infected cells and what type of antigen is this

A

T cytotoxic cells
endogenous antigen

145
Q

what is the marker for cytotoxic T cells

A

CD 8+

146
Q

what two substances do cytotoxic T cells release to kill cells

A

perforin and granzymes

147
Q

function of perforin

A

pore forming cytolytic protein that allows salt and water to enter cells and causes them to lyse

148
Q

function of granzymes

A

proteases which initiates DNA degradation and apoptosis

149
Q

how do T cytotoxic cells cause apoptosis (2 steps)

A
  1. Tc cells expresses Fas ligand which binds to Fas on target cells
  2. which activates caspase cascade to cause apoptosis
150
Q

what MHC does T cytotoxic cells detect

A

MHC I

151
Q

once activated what do cytotoxic T cells turn into (2)

A

effector or memory cells

152
Q

marker for T helper cells

A

CD 4+

153
Q

what is T cell polarisation and give two examples

A

antagonistic action of T helper cells eg Th1 and Th2 and Th17 and Treg

154
Q

what do Th17 and Tregs do

A

17= inflammation
Reg= tolerance

155
Q

what type of adaptive immunity do Th1 cells support

A

cell mediated

156
Q

what cells Th1 regulate (4)

A

monocytes, macrophages, NK and cytotoxic T cells

157
Q

overall action of Th1

A

eliminates cellular antigens

158
Q

what type of immunity do Th2 cells support

A

humoral immunity

159
Q

what cells Th2 regulate (3)

A

eosinophils, basophils, mast cells

160
Q

overall action of Th2 (3)

A

stimulate B cells, increase IgE antibody production by class switching B cells

161
Q

what r Tregs

A

principle cells in peripheral immune tolerance (tolerance)

162
Q

what is the key cytokine with mass anti-inflammatory action

A

IL 10

163
Q

where is Th17 located

A

mucosal membranes

164
Q

what is the principle cytokines of Th17 cells and what is its action

A

IL17
induces immune cells to produce IL 8

165
Q

three types of B cells

A

can be naive, effector or memory

166
Q

whats the mature B cell marker

A

CD 20

167
Q

what is the alternative name for effector B cells

A

plasma cells

168
Q

what 3 steps happens when memory B cells encounter their specific antigen?

A
  1. activated
  2. undergoes proliferation
  3. begin secreting IgG
169
Q

where does B cell activation occur

A

secondary lymphoid organs in cortex of lymph nodes mostly

170
Q

what r the two ways that B cells can be activated

A
  1. activated directly by internalising the antigen
  2. activated indirectly via APCs
171
Q

characteristic of B cells that r directly activated by antigens (3)

A

short lived B cells
rapid production
IgM releasing

172
Q

characteristic of B cells indirectly activated (3)

A

long-lived plasma cells
release IgG, E or A
higher affinity

173
Q

where do activated B memory cells go after an infection has been dealt with

A

back to secondary organ or to bone marrow

174
Q

where do B cells migrate to and from after activation

A

migrate from their lymphoid follicles to newly formed germinal centres

175
Q

what three changes do B cells undergo after activaation

A

somatic hypermutation, clonal expansion, class swtiching

176
Q

how is B cell affinity tested after somatic hypermutation? What happens to those with high affinity

A

Dendritic cells in germinal centres present the same antigen to the B cell to test its affinity- positive selection occurs for B cells with high affinity

177
Q

what is somatic hypermutation

A

point mutations in antibody which allows higher affinity binding to antigen

178
Q

what does the Fab region of an antibody bind to

A

epitope of the antigen

179
Q

what r Fab regions of an antibody determined by?

A

determined by a process called VDJ recombination during maturation in the bone marrow

180
Q

what is agglutination

A

using antibodies to cluster and bind pathogens together

181
Q

functions of antibodies 4

A

neutralisation of toxins
agglutination
opsonisation of pathogens
complement activation via the classical pathway

182
Q

what does the antibody Fc region stand for and what dose it bind to

A

fragment crystallisable region
binds to Fc receptors on immune cells surfaces

183
Q

what does the constant region of the antibody determine 2

A

antibody type and therefore effector function

184
Q

what r the 3 structural ways of labelling antibodies

A
  1. variable and constant region
  2. Fab and Fc region
  3. light and heavy chains (constant region= only heavy, variable= light and heavy)
185
Q

what is colostrum

A

initial part of breastmilk

186
Q

what antibodies does colostrum contain (3 and which one is the principle one)

A

IgA, IgM and IgG but IgA is the principle antibody

187
Q

what is lymphocytosis and what 2 types of infection cause this

A

raised lymphocyte levels
viral infections and intracellular bacterial infections but these r less common eg TB)

188
Q

where is IgA normally present in the body (3)

A

coats mucosal surfaces, colostrum and coats neonate gut

189
Q

form of IgA antibody

A

dimer

190
Q

form of IgM antibody

A

pentameric

191
Q

what antibody has highest capacity to activate complement

A

IgM

192
Q

what antibody is most abundant in blood

A

IgG

193
Q

how specific is IgM

A

not entirely specific to antigen

194
Q

how specific is IgG

A

highly specific

195
Q

which antibody can cross the placenta

A

IgG

196
Q

what antibody is important in secondary responses

A

IgG

197
Q

how many subclasses does IgG have?

A

4

198
Q

what cells does IgE bind to and how

A

mast cells and basophils
via Fc receptors

199
Q

tell mw about IgD function

A

not known

200
Q

what infections r IgE antibodies important for (2)

A

allergy and helminth

201
Q

what is the first antibody to respond to antigen exposure

A

IgM

202
Q

what happens to IgG levels in secondary response (2)

A

IgG levels increase rapidly and to a high level

203
Q

what is hypersensitivity

A

undesirable response to antigenic, allergenic or self material

204
Q

condition for hypersensitivity

A

requires pre-sensitisation state of the host

205
Q

what type of reaction is T1 and give an example

A

anaphylactic eg anaphylaxis

206
Q

what type of reaction is T2 and give an example

A

antibody-mediated eg pernicious anaemia

207
Q

what type of reaction is T3 and give one example

A

immune complex eg farmer’s lung

208
Q

what type of reaction is T4 and give one example

A

T cell mediated eg TB

209
Q

mechanism of T1 reaction and what is released

A

cross linking of antigen to IgE on mast cells/ basophils causes massive degranulation therefore, massive release of histamine

210
Q

what makes up a membrane attack complex (5) and what does a MAC do?

A

C5b, C6, C7, C8, C9, creates hole in bacterial cell membrane

211
Q

mechanism in T2 reaction and what are the two methods that this causes cell destruction

A

igM/ igG binds to self antigen on cell surface= cell destruction by the membrane attack complex and cellular mechanisms

212
Q

mechanism of T3 reaction and what does it cause

A

free IgG/IgA binds soluble antigen forming a circulating immune complex which causes inflammation

213
Q

mechanism of T4 reaction (include second exposure)

A

primary exposure: Th1 is activated by APCs and forms memory T cells
secondary exposure: memory T cell encountering antigen again, they activate macrophages causing tissue damage

214
Q

what cell is T4 reactions mediated by

A

Th1- T helper cell 1

215
Q

examples of T1 reaction 4

A

anaphylaxis
asthma
hay fever
dermatitis

216
Q

examples of T2 reaction (4)

A

autoimmune haemolytic anaemia
goodpastures’s syndrome
pernicious anaemia
RHEUMATIC FEVER

217
Q

examples of T3 reaction (2)

A

systemic lupus eyrthematosus
post-streptococcal glomerulonephritis

218
Q

examples of T4 reaction (4)

A

TB
graft vs host disease
MS
guillian-barre syndrome

219
Q

what is anaphylaxis classed as medically

A

a medical emergency that can be fatal

220
Q

what is treatment procedure for anaphylaxis (4)

A
  1. ABCDDE
  2. call help
  3. remove trigger
    4.IM 500mcg adrenaline
221
Q

what is the treatment if there is no response to anaphylaxis treatment after 5 minutes

A

repeat IM adrenaline

222
Q

what 3 things can cause autoimmunity to develop

A

thymic education failure (mismatch of immune tolerance)
failure of t regs (normally release IL 10)
CD4 activation against autoantigens

223
Q

what does treatment for autoimmunity involve (2)

A

reducing inflammation
suppressing the immune system

224
Q

2 examples of autoimmune conditions

A

SLE
MS

225
Q

what is central tolerance- better definition?

A

B and T cell receptors r tested against see antigens

226
Q

what 2 things happen to B cells in central tolerance that recognise self antigen

A

apoptosis or receptor editing

227
Q

what happens to T cells in central tolerance

A

T cells undergo positive and negative selection (+ recognise MHC molecules and - test affinity to self)

228
Q

what is peripheral tolerance and what cell tests this

A

peripheral tolerance= some low affinity self reactive T cells can escape the thymus to the periphery and r tested by dendritic cells.

229
Q

what happens to identified faulty T cells in peripheral tolerance

A

undergo apoptosis or are converted to Tregs

230
Q

4 features of autoimmunity

A

often relapsing remitting
damage/ destruction of tissues
altered organ growth/ function
generation of autoantibodies

231
Q

what is primary immunodeficiency, what types of disorders and give an example

A

those born with intrinsic defects in their immune system
rare and mostly genetic disorders
eg SCID (where T and B cells lose functionality)

232
Q

what is secondary immunodeficiency, what is it referred to as

A

acquired immunodeficiency and referred to as immunosuppression

233
Q

define what occurs in immunosuppression

A

production is negated or blocked

234
Q

what can induce secondary immunodeficiency? 2

A

drugs eg steroids
cancers of bone marrow and blood eg leukaemia

235
Q

explain profound immunodeficiency regarding HIV and AIDs

A

HIV has a cell tropism for CD4+ which destroys them
once CD4 cell count is bellow 200 cells/uL there is profound immunodeficiency= defines development of AIDS

236
Q

what is the principle of vaccination (5 key points, 1 definition)

A

controlled and safe exposure to a part of a pathogen that is immunogenic and will induce immunological memory with little to no harm to the host

237
Q

what is negative phase related to vaccinations

A

period after initial antigen exposure where ones immunity is actually lower than before encountering the antigen

238
Q

compare active and passive immunity negative phase

A

active= negative phase and passive= no negative phase

239
Q

compare active and passive immunity boosters

A

booster effect on subsequent dose for active immunity but in passive, the antibodies r eliminated so there is no boost

240
Q

what is the key cytokine for resolution of allergic inflammation

A

INF gamma

241
Q

4 functions of IL4

A

IgE class switching
Th2 polorisation
promotes eosinophils to enter tissues and mucous secretions
activates B cells to differentiate into plasma cells

242
Q

name all the pro-inflammatory cytokines (9)

A

1, 2, 3, 5, 6, 8, 12, TNF alpha, Interferon gamma

243
Q

name all the anti-inflammatory cytokines (2)

A

4, 10

244
Q

main source of IL1 and function

A

macrophages
induces fever

245
Q

main source of IL2 and function

A

Th1 cells
stimulates growth and differentiation of T cells

246
Q

main source of IL3 and function

A

activated T helper cells
stimulates differention and proliferation of myeloid pregenitor cells

247
Q

main source of IL4 and function

A

Th2 cells
stimulates proliferation and differentiation of B cells

248
Q

main source of IL5 and function

A

Th2 cells
stimulates production of eosinophils

249
Q

main source of IL6 and function

A

macrophages and Th2
stimulates differentiation of b cells and induces fever

250
Q

What is chemotaxis and what two things can do this

A

attraction and movement of macrophages towards a chemical signal
cytokines and chemokines

251
Q

main source of IL8 and function

A

macrophages
neutrophil chemotaxis

252
Q

main source of IL10 and function

A

th2 cells
inhibits th1 cytokine production

253
Q

main source of IL12 and 2 functions

A

dendritic cells, macrophages, b cells (APCs)
activates NK cells and stimulates differentiation of naive T cells into Th1 cells

254
Q

main source of TNF alpha and functions (2)

A

macrophages
induces fever, neutrophil chemotaxis

255
Q

main source of Interferon gamma and function

A

th1 cells
activates macrophages and NK cells

256
Q

what is a complement (3- what is it, where is it synthesised, what form does it circulate in)

A

an acute phase protein synthesised by the liver and circulates in an inactive form

257
Q

name the three pathways of complement

A

classical, B lectin and and alternative pathway

258
Q

what is the function of C3 convertase

A

cleaves C3 into C3a and C3b

259
Q

what is the product of the 3 complement pathways

A

C3 convertase

260
Q

what activates the classical pathways

A

antigen- antibody complex (IgM/G)

261
Q

what activates the alternative pathways

A

when C3b in plasma directly binds to pathogen surfaces and activates the cascade

262
Q

what activates the MB lectin pathway

A

activated by mannose binding lectin (MBL) binding on mannose on pathogen’s surface

263
Q

what is mannose

A

mannose is a pathogen surface carbohydrate that is not present on human cell

264
Q

what r the 3 main products of the complement pathways (3)

A

mainly C3a, C5a, C3b

265
Q

what does C3b do

A

opsonises pathogens

266
Q

what does C3a do (2)

A

inflammation and chemotaxis

267
Q

what is CD3 a marker of?

A

signalling component of T cell receptor

268
Q

what is CD4 a marker of? Where is this found (1) and what is its significance pathologically

A

co-receptors for MHC II
found on helper T cells
used by HIV to enter T cells

269
Q

what is CD8 a marker of? Where is this found (2)

A

co-receptor for MHC I
found on subset of myeloid dendritic cells and on all T cells

270
Q

what is CD14 a marker of?

A

surface marker for macrophages

271
Q

what is CD16 a marker of?

A

bind to Fc portion of IgG antibodies

272
Q

what is CD56 a marker of?

A

unique marker for NK cells

273
Q

what is CD95 a marker of?

A

acts as FAS receptor, involved in apoptosis

274
Q

main marker for a T reg cell

A

CD 28

275
Q

four examples of immune based therapies

A

monoclonal antibodies, cytokines, IV immunoglobulins, immunosuppressive drugs

276
Q

why r cytokines often the drug target for immunity

A

because cytokines regulate the immune system

277
Q

what do HLAs stand for and compare to MHC

A

human leukocyte antigen
HLA r specific to humans only as other animals have MHCs but HLA is synonymous to MHC

278
Q

which HLA associates correspond to MHC I (3)

A

A, B, C

279
Q

which HLA associates correspond to MHC II (4)

A

HLA-DR, DQ, DP and DM

2A content- Sameera (21 decks)

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