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1st Year Med > Immunology > Flashcards

Immunology Flashcards

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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
what are B cell receptors?
an antibody (surface immunoglobulin)
26
what are the 5 stages of the adaptive immune response?
antigen recognition, lymphocyte activation, antigen elimination, contraction (homeostasis), memory
27
explain the structure of an antibody
bivalent monomer: 4 polypeptide chains (2 light, 2 heavy) antigen binding fragment (Fab) crystalline fragment (Fc) - binds cells/complement
28
what are the 6 functions of antibodies?
agglunitation opsonisation neutralisation cytotoxicity inflammation complement activation (ICONAC)
29
explain agglutination
enhances phagocytosis and reduces number of infectious units to be dealt with
30
explain opsonisation
coating of antigen with antibody to enhance phagocytosis
31
explain antibody neutralisation
blocks adhestion of bacteria and viruses to mucosa blocks active site of toxin
32
explain antibody-dependant cell-mediated cytotoxicity
antibodies attached to target cell non specific immune system cells come and destroy it
33
explain antibody inflammation
cell disruption by complement, which attracts phagocytic/defensive immune cells
34
what do helper T cells do in cell mediated immunity?
help B cells help cytotoxic T cells direct innate responses
35
explain the structure and subdivision of T cells in relation to CD(number)'s
T cell receptor on surface, CD3 identifies cells further subdivided by expression of one of 2 surface molecules: CD4 or CD8
36
what do CD4 T helper cells do?
recognised antigen presented in MHC 2 on antigen-presenting cells surface and 'help' them
37
what do CD8 cytotoxic T cells do?
recognise antigen presented in MHC 1 on many cell types and can be induced to kill
38
name 3 signals T cells need for activation
antigen presented in context of MHC surface molecule costimulation soluble molecules (cytokines)
39
how do T cells 'help' B cells?
antigen recognition -> T cell effector molecule expression -> B cell activation and proliferation -> differenciation to resting memory cells and antibody-secreting plasma cells
40
what are the 2 functions of helper T lymphocytes?
help the antigen-driven maturation of B and T cells facilitate/magnify the interaction between APCs and immunocompetent lymphocytes
41
what are the steps of the helper T lymphocyte mechanism?
helper T lymphocyte (Th) interacts through antigen-specific and antigen-independant mechanisms -> undergoes differenciation -> mature Th interacts with plasma or T-effector cells
42
what 3 things may cause inflammation?
physical/chemical damage infectious agent antigen challenge
43
what are the 3 aims of inflammation?
expel foreign infection prevent metastasis structural and functional repair
44
what are the 5 clinical features of inflammation?
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
how does inflammation promote healing of damage?
mobilises effector cells and molecules to site creates environment suitable for repair
46
explain the negatives of inflammation
can become out of proportion with threat more damage than trauma would've caused (loss of organ/tissue function)
47
what is the outcome of sterilising immunity?
recovery
48
what is the outcome of non-sterilising immunity?
chronic infection
49
what is the outcome of immune failure?
death
50
what key defenses are necessary in mycobacterium tubercullosis?
cell mediated immunity macrophages controlling cell T cell production of interferon gamma cytokines
51
what does M.tb cause?
apical destruction
52
when does M.tb grow best?
high oxygen levels
53
what will lungs affected by M.tb contain?
granulomas, caseous necrosis, lymphocytes, epitheloid cells
54
explain how tb spreads in cavitary tb
cavities open into bronchi allowing M.tb spread through coughing
55
how has M.tb adapted to survive phagocytosis?
alters phagocyte and coats it with coronin and inhibits its ability to bind to a lysosome neutralises phagosomal acidification
56
name the interleukins involved in the M.tb immune response
Interleukin 12 and 18
57
what is unusual about HIVs life cycle?
its a retrovirus (genome reverse transcribed and integrated into host genome)
58
what cells keep HIV 'in check'?
cytotoxic CD8 T cells
59
what relationship do CD8 response and viral set point have?
greater CD8 response results in lower viral set point
60
what antibody initially defends against HIV?
free gp-41 specific non-neutralising IgM
61
what are the symptoms of dengue fever?
fever, rash, mild headache
62
what damage can severe dengue fever do?
plasma leakage multi organ impairment haemmorhage
63
what 2 antibodies accumulate during the dengue fever immune response?
initially IgM then IgG
64
explain the difference in secondary dengue infections from the same/different serotypes
same serotype - increased protective immunity different serotype - increased chance of severity
65
name some examples of type 1 hypersensetivity
hay fever, food allergies, pet allergies, insect bites
66
what cells cause type 1 hypersensetivity?
IgE and mast cells
67
what happens to mast cells during type 1 hypersensetivity?
degranulation releasing histamine and prostoglandins
68
which antibodies target type 2 and 3 hypersensetivity?
IgM and IgG
69
what cells are involved in type 4 hypersensetivity?
CD8 cytotoxic T cells CD4 T cells
70
what is the difference between organ specific and non-organ specific autoimmune diseases?
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
define autoimmunity
misdirected immune response, attacks our own bodies as opposed to pathogens
72
what is the pathway to autoimmunity?
genetic factors or infection/environmental exposure -> immune regulation -> autoimmunity
73
name 4 organ-specific autoimmune disorders
type 1 diabetes goodpastures syndrome MS graves disease
74
name 3 systemic autoimmune diseases
rheumatoid arthritis sclerodema lupus
75
what happens during graves disease?
non-regulated auto-antibodies bind to thyroid stimulating hormones (TSH) causing hyperthyroidism
76
what occurs during transplant rejection?
T cells activated against donor transplantation antigens (CD4 and CD8) stimulation in peripheral lymphoid tissues antibody production, complement activation
77
what are the 4 types of transplant rejections?
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
what is primary immunodeficiency?
congenital, resulting from genetic defects
79
what is secondary immunodeficiency?
acquired - result of other diseases or conditions
80
name 3 secondary immunodeficiency diseases
HIV malnutrition immunosuppression
81
name 3 examples of primary immunodeficiency diseases
allergies autoimmunity abnormal lymphocyte
82
how do B cell deficiencies present?
reduced/absent follicles and germinal centres in lymphoid organs reduced Ig serum levels
83
how do T cell deficiencies present?
reduced T cell zones in lymphoid organs reduced DTH reactions to common antigens
84
name 3 combined immunodeficiencies and what causes them
TB+ SCID - common gamma chain deficiency TB- SCID - adenosine deaminase deficiency less profound - CD40L deficiency
85
describe the characteristics of X-linked SCID
'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
what does ADA-SCID deplete?
T/B/NK cells, basal expression in all cells, enhanced by thymocytes
87
explain the characteristics and causes of alopecia
FoxN1 deficiency, hair and epithelial thymus fail to develop -> ineffective thymus -> no T cells B cells normal but no help
88
what 3 common antibodies are deficient in FoxN1 deficiency?
brutons tyrosine kinase CD40L IgA
89
what occurs in humoral/B cell defects?
lack of antibody recurrent sepsis bacterial infections in airways GI failure
90
explain what an IgA deficiency could cause
an IL deficiency - cytokines need to mature lymphocyte into mature IgA plasma cell
91
what are 3 common phagocyte defects?
neutrophil function respiratory burst (CGD) mendelian susceptibility to mycobacterial disease (MSMD)
92
which IL is involved in familial mediterranean fever (FMF)?
IL-1
93
name the 4 things occuring in immune regulatory failure
loss of central and peripheral tolerance molecular mimicry innapropriate activation
94
explain the pathogenesis of autoimmune diseases
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
explain immune mediated inflammatory response
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
name 2 autoimmune diseases that contain T cell specific auto-antigens which produces an anti-host response
graves - T cells to thyroid follicular epithelial cells myasthenia gravis - T cells to ACl receptor

1st Year Med (52 decks)

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