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1st Year Med > Immunology > Flashcards

Immunology Flashcards

1
Q

name physical barriers in which pathogens can breach

A

lungs, GI tract, reproductive tract, skin

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2
Q

where do T-lymphocytes mature?

A

thymus

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3
Q

what 3 cells leave the blood and take long-term residency in tissues?

A

dendritic cells, macrophages and mast cells

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4
Q

where do B and T lymphocytes spend most of their life?

A

secondary lymph organs

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5
Q

name the 5 secondary lymph organs

A

peyers patches, appendix, spleen, lymph nodes, tonsil

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6
Q

name the WBCs in the adaptive immune system

A

B and T lymphocytes
(other WBCs all innate)

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7
Q

what do B and T lymphocytes produce in the adaptive immune response?

A

B - antibodies
T - effector T cells

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8
Q

what are the 3 ways complement can be activated and how does each one work?

A

classic - antigen/antibody complexes
MB-lectin - lectin binding to pathogen surfaces
alternate - pathogen surfaces

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9
Q

what 3 things occur after complement activation?

A

inflammatory cell recruitment
opsonisation of pathogens
killing of pathogens

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10
Q

what is complement?

A

a cascade of proteins in serum

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11
Q

what is the mechanism pathway of innate immunity?

A

infection -> recognition by performed nonspecific effectors -> infectious agent removal

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12
Q

what is the mechanism pathway of the early induced response?

A

infection -> recruitment of effector cells -> recognition activation of effector cells -> infectious agent removal

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13
Q

what is the mechanism pathway of the adaptive response?

A

infection -> transport antigen to lymphoid organs -> recognition by naive B/T cells -> production of effector cells -> infectious agent removal

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14
Q

describe the characteristics of neutrophils

A

short lived (6-12 hours)
first line of defense
phagocytose pathogens
release soluble mediators

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15
Q

what do 1st degree granules in neutrophils contain?

A

bactericidal enzymes (lysozyme, neutral proteases, acid hydrolases, myeloperoxidase)

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16
Q

what do 2nd degree granules in neutrophils contain?

A

lysozyme, collagenase, lactoferrin, cathepsin B

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17
Q

what are the 4 steps to innate cells migrating to infection sites?

A

rolling adhesion, tight binding, diapedesis, migration

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18
Q

how do macrophages act on pathogens?

A

they reorganise their actin cytoskeleton to engulf bacteria digested in the cell

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19
Q

what are pseudopodia?

A

macrophage extentions that engulf apoptotic cells

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20
Q

describe the characteristics of macrophages

A

developed in tissues from precursors
active phagocytic cells
activated by inflammation
long lived

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21
Q

where is the antigen concentrated when arriving via lymph?

A

lymph nodes

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22
Q

describe the humoral adaptive immune response

A

antibody (from B cells) mediated extracellular attack

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23
Q

describe the cell mediated adaptive immune response

A

T cell coordinated intracellular attack

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24
Q

where do B cells mature?

A

bone marrow

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25
Q

what are B cell receptors?

A

an antibody (surface immunoglobulin)

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26
Q

what are the 5 stages of the adaptive immune response?

A

antigen recognition, lymphocyte activation, antigen elimination, contraction (homeostasis), memory

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27
Q

explain the structure of an antibody

A

bivalent monomer: 4 polypeptide chains (2 light, 2 heavy)
antigen binding fragment (Fab)
crystalline fragment (Fc) - binds cells/complement

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28
Q

what are the 6 functions of antibodies?

A

agglunitation
opsonisation
neutralisation
cytotoxicity
inflammation
complement activation
(ICONAC)

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29
Q

explain agglutination

A

enhances phagocytosis and reduces number of infectious units to be dealt with

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30
Q

explain opsonisation

A

coating of antigen with antibody to enhance phagocytosis

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31
Q

explain antibody neutralisation

A

blocks adhestion of bacteria and viruses to mucosa
blocks active site of toxin

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32
Q

explain antibody-dependant cell-mediated cytotoxicity

A

antibodies attached to target cell
non specific immune system cells come and destroy it

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33
Q

explain antibody inflammation

A

cell disruption by complement, which attracts phagocytic/defensive immune cells

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34
Q

what do helper T cells do in cell mediated immunity?

A

help B cells
help cytotoxic T cells
direct innate responses

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35
Q

explain the structure and subdivision of T cells in relation to CD(number)’s

A

T cell receptor on surface, CD3 identifies cells
further subdivided by expression of one of 2 surface molecules: CD4 or CD8

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36
Q

what do CD4 T helper cells do?

A

recognised antigen presented in MHC 2 on antigen-presenting cells surface and ‘help’ them

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37
Q

what do CD8 cytotoxic T cells do?

A

recognise antigen presented in MHC 1 on many cell types and can be induced to kill

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38
Q

name 3 signals T cells need for activation

A

antigen presented in context of MHC
surface molecule costimulation
soluble molecules (cytokines)

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39
Q

how do T cells ‘help’ B cells?

A

antigen recognition -> T cell effector molecule expression -> B cell activation and proliferation -> differenciation to resting memory cells and antibody-secreting plasma cells

40
Q

what are the 2 functions of helper T lymphocytes?

A

help the antigen-driven maturation of B and T cells
facilitate/magnify the interaction between APCs and immunocompetent lymphocytes

41
Q

what are the steps of the helper T lymphocyte mechanism?

A

helper T lymphocyte (Th) interacts through antigen-specific and antigen-independant mechanisms -> undergoes differenciation -> mature Th interacts with plasma or T-effector cells

42
Q

what 3 things may cause inflammation?

A

physical/chemical damage
infectious agent
antigen challenge

43
Q

what are the 3 aims of inflammation?

A

expel foreign infection
prevent metastasis
structural and functional repair

44
Q

what are the 5 clinical features of inflammation?

A

redness (rubor) - vasodilation
heat (calor) - vasodilation and fever
swelling (tumour) - ECM fluid
pain (dolor) - pain mediators (bradykinin/serotonin)
function loss (functio laesa) - inhibited limb movement

45
Q

how does inflammation promote healing of damage?

A

mobilises effector cells and molecules to site
creates environment suitable for repair

46
Q

explain the negatives of inflammation

A

can become out of proportion with threat
more damage than trauma would’ve caused (loss of organ/tissue function)

47
Q

what is the outcome of sterilising immunity?

A

recovery

48
Q

what is the outcome of non-sterilising immunity?

A

chronic infection

49
Q

what is the outcome of immune failure?

A

death

50
Q

what key defenses are necessary in mycobacterium tubercullosis?

A

cell mediated immunity
macrophages controlling cell
T cell production of interferon gamma
cytokines

51
Q

what does M.tb cause?

A

apical destruction

52
Q

when does M.tb grow best?

A

high oxygen levels

53
Q

what will lungs affected by M.tb contain?

A

granulomas, caseous necrosis, lymphocytes, epitheloid cells

54
Q

explain how tb spreads in cavitary tb

A

cavities open into bronchi allowing M.tb spread through coughing

55
Q

how has M.tb adapted to survive phagocytosis?

A

alters phagocyte and coats it with coronin and inhibits its ability to bind to a lysosome
neutralises phagosomal acidification

56
Q

name the interleukins involved in the M.tb immune response

A

Interleukin 12 and 18

57
Q

what is unusual about HIVs life cycle?

A

its a retrovirus (genome reverse transcribed and integrated into host genome)

58
Q

what cells keep HIV ‘in check’?

A

cytotoxic CD8 T cells

59
Q

what relationship do CD8 response and viral set point have?

A

greater CD8 response results in lower viral set point

60
Q

what antibody initially defends against HIV?

A

free gp-41 specific non-neutralising IgM

61
Q

what are the symptoms of dengue fever?

A

fever, rash, mild headache

62
Q

what damage can severe dengue fever do?

A

plasma leakage
multi organ impairment
haemmorhage

63
Q

what 2 antibodies accumulate during the dengue fever immune response?

A

initially IgM then IgG

64
Q

explain the difference in secondary dengue infections from the same/different serotypes

A

same serotype - increased protective immunity
different serotype - increased chance of severity

65
Q

name some examples of type 1 hypersensetivity

A

hay fever, food allergies, pet allergies, insect bites

66
Q

what cells cause type 1 hypersensetivity?

A

IgE and mast cells

67
Q

what happens to mast cells during type 1 hypersensetivity?

A

degranulation releasing histamine and prostoglandins

68
Q

which antibodies target type 2 and 3 hypersensetivity?

A

IgM and IgG

69
Q

what cells are involved in type 4 hypersensetivity?

A

CD8 cytotoxic T cells
CD4 T cells

70
Q

what is the difference between organ specific and non-organ specific autoimmune diseases?

A

organ specific - attack on self-antigens of given organ damaging its structure and function
non-specific - widespread self-antigens are attacked damaging blood vessels/nuclei etc.

71
Q

define autoimmunity

A

misdirected immune response, attacks our own bodies as opposed to pathogens

72
Q

what is the pathway to autoimmunity?

A

genetic factors or infection/environmental exposure -> immune regulation -> autoimmunity

73
Q

name 4 organ-specific autoimmune disorders

A

type 1 diabetes
goodpastures syndrome
MS
graves disease

74
Q

name 3 systemic autoimmune diseases

A

rheumatoid arthritis
sclerodema
lupus

75
Q

what happens during graves disease?

A

non-regulated auto-antibodies bind to thyroid stimulating hormones (TSH) causing hyperthyroidism

76
Q

what occurs during transplant rejection?

A

T cells activated against donor transplantation antigens (CD4 and CD8)
stimulation in peripheral lymphoid tissues
antibody production, complement activation

77
Q

what are the 4 types of transplant rejections?

A

hyperacute - existing antibodies in hosts blood
acute cellular - T cells destroy graft parenchyma
acute humoral - antibodies damage graft vasculature
chronic - associated with parenchymal fluids

78
Q

what is primary immunodeficiency?

A

congenital, resulting from genetic defects

79
Q

what is secondary immunodeficiency?

A

acquired - result of other diseases or conditions

80
Q

name 3 secondary immunodeficiency diseases

A

HIV
malnutrition
immunosuppression

81
Q

name 3 examples of primary immunodeficiency diseases

A

allergies
autoimmunity
abnormal lymphocyte

82
Q

how do B cell deficiencies present?

A

reduced/absent follicles and germinal centres in lymphoid organs
reduced Ig serum levels

83
Q

how do T cell deficiencies present?

A

reduced T cell zones in lymphoid organs
reduced DTH reactions to common antigens

84
Q

name 3 combined immunodeficiencies and what causes them

A

TB+ SCID - common gamma chain deficiency
TB- SCID - adenosine deaminase deficiency
less profound - CD40L deficiency

85
Q

describe the characteristics of X-linked SCID

A

‘bubble boy’ disease
mutations in cytokine receptors IL-2Ry chain
T cells/NK cells fail, B cells normal but no help for efficient antibody responses

86
Q

what does ADA-SCID deplete?

A

T/B/NK cells, basal expression in all cells, enhanced by thymocytes

87
Q

explain the characteristics and causes of alopecia

A

FoxN1 deficiency, hair and epithelial thymus fail to develop -> ineffective thymus -> no T cells
B cells normal but no help

88
Q

what 3 common antibodies are deficient in FoxN1 deficiency?

A

brutons tyrosine kinase
CD40L
IgA

89
Q

what occurs in humoral/B cell defects?

A

lack of antibody
recurrent sepsis
bacterial infections in airways
GI failure

90
Q

explain what an IgA deficiency could cause

A

an IL deficiency - cytokines need to mature lymphocyte into mature IgA plasma cell

91
Q

what are 3 common phagocyte defects?

A

neutrophil function
respiratory burst (CGD)
mendelian susceptibility to mycobacterial disease (MSMD)

92
Q

which IL is involved in familial mediterranean fever (FMF)?

A

IL-1

93
Q

name the 4 things occuring in immune regulatory failure

A

loss of central and peripheral tolerance
molecular mimicry
innapropriate activation

94
Q

explain the pathogenesis of autoimmune diseases

A

susceptible genes causes a failure in self-tolerance resulting in a persistance of functional self-reactive lymphocytes
in the event of an environmental trigger (infection/injury) these self-reactive lymphocytes will activate causing immune responses against self-tissues

95
Q

explain immune mediated inflammatory response

A

chronic diseases with prominent inflammation caused by failure in tolerance or regulation
results from immune responses target self antigens or microbial antigens
may be caused by T-cells or antibodies
may be systemic or organ specific

96
Q

name 2 autoimmune diseases that contain T cell specific auto-antigens which produces an anti-host response

A

graves - T cells to thyroid follicular epithelial cells
myasthenia gravis - T cells to ACl receptor

1st Year Med (52 decks)

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