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2A CLINICAL SCIENCES > Immunology > Flashcards

Immunology Flashcards

1
Q

Innate immunity

A

-front-line of defence against any pathogen that attempts to attack the body
-non-specific, standardised, rapid
-no immunological memory
-does not depend on lymphocytes
-present from birth
-primitive (spread across species)

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2
Q

Adaptive immunity

A

-specific immune response which creates immunological memory and thus leads to an enhanced response to future encounters with the same pathogen
-mircrobes evade innate immunity, intracellular viruses & bacteria able to hide from innate immunity, need memory to specific antigen
-specificity, immunological memory, self/non-self recognition
-response and memory specific to antigen - quicker secondary response
-requires lymphocytes

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3
Q

Haematopoietic pluripotent stem cell

A

-haemocytoblast
-stem cell that every blood cell in the body originates from

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4
Q

Mononuclear leukocytes

A

Leukocytes with one nucleus

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5
Q

Polymorphonuclear leukocytes

A

Leukocytes with more than one nucleus

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6
Q

Examples of mononuclear leukocytes

A

Monocytes (kidney-shaped nuclei)
T cells
B cells
(lymphocytes)

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7
Q

Examples of polymorphonuclear leukocytes

A

Neutrophils
Eosinophils
Basophils

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8
Q

Neutrophils

A

-phagocytosis (innate immunity)
-2 main intracellular granules - primary lysosomes, secondary granules
-primary lysosomes - can kill microbes by secreting toxic substances

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9
Q

Monocytes

A

-phagocytosis (innate immunity)
-Ag presentation (adaptive immunity)
-differentiate into macrophages in tissues
-primary role is to remove foreign microbes or dead self matter

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10
Q

Macrophages

A

-phagocytosis (innate immunity)
-Ag presentation (adaptive immunity)
-reside in tissues
-primary role is to remove foreign (microbes) and self (dead/tumour cells)
-present Ag to T-cells

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11
Q

What is the lifespan of macrophages?

A

Months/years

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12
Q

Macrophages in the liver

A

Kupffer cells

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13
Q

Macrophages in the brain

A

Microglia

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14
Q

Eosinophil

A

-mainly associated with parisitic infections & allergic reactions
-activates neutrophils, induces histamine release from mast cells & promotes brocnhospasm

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15
Q

What stains eosinophil granules?

A

Acidic dyes (eosin)

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16
Q

Lifespan of macrophages

A

Months/years

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17
Q

Lifespan of eosinophils

A

8-12 days

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18
Q

Basophils

A

-mainly involved in immunity to parasitic infections & allergic reactions
-similar to mast cells
-binding of IgE to receptor causes de-granulation releasing histamine -> allergic reactions

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19
Q

What stains basophil granules?

A

Basic dyes

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20
Q

Lifespan of basophils

A

2 days

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21
Q

Mast cells

A

-precursor in blood
-mast cells only in tissues
-similar to basophils
-binding of IgE to receptor causes de-granulation releasing histamine -> allergic reactions

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22
Q

T lymphocytes

A

-major role in adaptive immunity
-recognise peptide Ag displayed on APCs
-T cells recognise 1 antigen -> T cell binds to antigen -> clonal selection to produce effector & memory T cells (effector T cells activate other immune cells, eg. macrophages)
-T cells do not bind to free antigens - the antigen must be associated with the MHC - MHC presents antigens to T cells
-T cells produce cytokines

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23
Q

Lifespan of T cells

A

Hours-years

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24
Q

Where do T cells originate?

A

Stem cells in bone marrow

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25
Q

Where do T cells mature?

A

Thymus

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26
Q

Where are T cells found?

A

Blood
Lymph nodes
Spleen

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27
Q

Purpose of CD3 sites on T cells

A

-do not bind to Ag
-instead, after Ag binds to cell, CD3 site sends signal into the cell nucleus

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28
Q

What do T cells require for activation?

A

-2 signals
-signal 1 occurs when TCR comes together with an MHC bound antigen

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29
Q

What are the 4 main types of T cell?

A

T helper cells - CD4+ve - help B cells are antibody, activate macrophages & natural killer cells, help development of cytotoxic T cells (help activate B cells & cytotoxic T cells)

Cytotoxic T cell - CD8+ve - kill cells directly - recognise & kill infected host cells - release perforin that causes cells to lyse

T regulator/suppressor cells - CD4+ve - regulate/suppress immune responses

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30
Q

TH1 vs TH2 cells

A

TH1 - help immune response with intracellular pathogens

TH2 - help immune response with extracellular pathogens

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31
Q

What cytokines do TH1 cells produce?

A

IL-2
y-inteferon
TNFB

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32
Q

What cytokines do TH1 cells produce?

A

IL-4, -5, -6, -10, -13

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33
Q

What cytokines do TREG cells produce?

A

IL-10
TGF-B
IL-35
(down regulate other T cell subsets)

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34
Q

B lymphocytes

A

-major role in adaptive immunity
-recognise Ag displayed by APC
-differentiate into plasma cells

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35
Q

Lifespan of B lymphocytes

A

Hours-years

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36
Q

Where are B lymphocytes produced?

A

Bone marrow

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37
Q

Where do B lymphocytes mature?

A

Bone marrow

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38
Q

Where are B lymphocytes found?

A

Blood, lymph nodes, spleen

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39
Q

What is the role of plasma cells?

A

Produce antibodies

40
Q

What do antibodies do?

A

-immunoglobulins - soluble
-hallmark of adaptive immunity - they bind to a specific Ag on a pathogen
-attach to pathogens
-neutralise pathogen
-cause opsonization & agglutination
-cause phagocytosis of pathogen to occur
-antibody-dependent cellular cytotoxicity
-complement activation

41
Q

Opsonization

A

Opsonins tag pathogens for elimination by phagocytosis

42
Q

Antibody-dependent cellular cytotoxicity

A

-pathogen is coated with antibodies
-white blood cell (NK cell) bind to the antibodies and release substances that kill the pathogen

43
Q

What are B memory cells?

A

-plasma cells
-which remain in the blood after an infection
-they can produce antibodies to a specific antigen within a short amount of time if that antigen is found within the body again

44
Q

Natural killer cells

A

-15% of lymphocytes
-found in spleen, tissues
-recognise & kill by apoptosis
-kill virus infected cells & tumour cells

44
Q

Natural killer cells

A

-15% of lymphocytes
-found in spleen, tissues
-recognise & kill by apoptosis
-kill virus infected cells & tumour cells

45
Q

What are soluble factors of the immune system?

A

-complement
-antibodies
-cytokines
-chemokines

46
Q

Complement factors

A

-facilitate the uptake & destruction of pathogen by phagocytic cells
-mode of action = direct lysis, attract more leukocytes to site of infection, coat invading organisms
-classical - Ab bound to microbe
-alternative - C bound to microbe

47
Q

What type of molecule are immunoglobulins?

A

Glycoproteins

48
Q

What are the 5 classes of Igs?

A

IgG
IgA
IgM
IgD
IgE

49
Q

IgG

A

-predominant in human serum
-70-75% of total Ig in serum
-crosses placenta

50
Q

IgA

A

-15% of Ig in serum
-predominant Ig in mucous secretions, eg. saliva, milk, bronchiolar secretions

51
Q

IgM

A

-accounts for 10% of Ig in serum
-mainly found in blood
-large so cannot cross endothelium
-mainly part of primary response - initial contact with Ag

52
Q

IgD

A

-accounts for 1% of Ig in serum
-a transmembrane monomeric form is present on mature B cells

53
Q

IgE

A

-accounts for ~0.05% of Ig in serum
-basophils & mast cells express an IgE-specific receptor that has high affinity or IgE - binding triggers histamine release
-associated with allergic response & defence against parasitic infections

54
Q

Human serum

A

Fluid that remains once clotting factors are removed from blood plasma

55
Q

Definition of antibody

A

-Ab
-protein produced in response to an antigen
-can only bind with the antigen that induced its formation - specificity

56
Q

Definition of antigen

A

-Ag
-molecule that reacts with preformed antibody and specific receptors on T and B cells

57
Q

Epitope

A

The part of the antigen that binds to the antibody/receptor binding site

58
Q

Affinity

A

Measure of binding strength between an epitope and an antibody binding site - the higher the affinity the better

59
Q

Cytokines

A

-proteins secreted by immune & non-immune cells
-substances produced by one cell that influence the behaviour of another -> affecting intercellular communication

60
Q

Name 4 types of cytokine

A

Interferons
Interleukins
Colony stimulating factors
Tumour necrosis factors

61
Q

Inteferons

A

-IFN
-induce a state of antiviral resistance in uninfected cells
-limit spread of viral infection

62
Q

Interleukins

A

-IL
-produced by many cells (over 30 types)
-cause cells to divide, to differentiate, to secrete factors

63
Q

Colony stimulating factors

A

-CSF
-involved in directing the division & differentiation of bone marrow stem cells (precursors of leukocytes

64
Q

Tumour necrosis factors

A

-mediate inflammation & cytotoxic reactions

65
Q

Chemokines

A

-40 proteins that direct movement of leukocytes from bloodstream -> tissues/lymph organs
-by binding to specific receptors on cells
-attract leukocytes to sites of infection/inflammation

66
Q

Types of leukocyte

A

Granulocytes - neutrophils, eosinophils, basophils
Monocytes
Lymphocytes - B cells, T cells

(white blood cells)

67
Q

What is innate immunity comprised of?

A

Physical & chemical barriers
Phagocytic cells - neutrophils, macrophages
Serum proteins - complement, acute phase

68
Q

Innate immunity - anatomical barriers

A

Skin - dermis, epidermis
Sebum - skin secretions
Intact skin - prevents penetration, prevents growth

69
Q

Components of mucous membranes - physical barrier

A

-saliva
-tears - lysozyme in tears & other secretions
-low pH & commensals of vagina
-mucous secretions
-mucous - entrapment
-clila - beating removes microbes
-commensal colonies - attachments, nutrients - prevent colonisation and invasion by pathogens

70
Q

Physiological barriers to pathogens

A

Temperature (chickens have high body temp. - anthrax resistant)
Fever - inhibits micro-organism growth
-pH
-gastric acidity (neonate stomach less acid than adult - susceptible to infection)

71
Q

Inflammation

A

-series of reactions
-that brings cells & molecules of the immune system
-to the site of infection/damage

72
Q

What is the response to a barrier being breached (tissue damage/infection)?

A

-stop bleeding - coagulation
-acute inflammation- leukocyte recruitment
-kill pathogens, neutralise toxins, limit pathogen spread
-clear pathogens/dead cells - phagocytosis
-proliferation of cells to repair damage
-remove blood clot - remodel extracellular matrix
-re-establish normal structure/function of tissue

73
Q

Hallmarks of inflammation

A

-increased blood supply
-increased vascular permeability
-increased leukocyte trans-endothelial migration - extravasation

74
Q

Extravasation

A

-discharge/escape
-as of blood
-from a vessel into the tissue

(usually lymph from blood into tissues)

75
Q

Acute inflammation

A

-complete elimination of a pathogen followed by resolution of damage, disappearance of leukocytes & full regeneration of tissue
-neutrophil mediated

76
Q

Chronic inflammation

A

-persistent, unresolved inflammation
-macrophage mediated

77
Q

Complement system

A

-cascade
-comprised of a distinct number of plasma proteins which react to opsonize pathogens & induce a series of inflammatory responses that help to fight infection

78
Q

What can Cā€™ (complement) do?

A

-lyse microbes directly - membrane attack complex
-increase chemotaxis - migration of immune cells towards source of stimulus through detection of the direction & intensity of an extracellular chemical gradient
-opsonization - C3b

79
Q

Phagocytosis stages

A

1)Binding
2)Engulfment
3)Phagosome formation - pathogen digested & vesicle forms around pathogen
4)Lysosome fusion - phagolysosome - lysozymes digest pathogen material
5)Membrane disruption
6)Antigen presentation/secretion

80
Q

What part of adaptive immunity kills intracellular microbes?

A

Cell mediated - T cells

81
Q

What part of adaptive immunity kills extracellular microbes?

A

Humoral (Ab) - B cells

82
Q

Major histocompatibility complex

A

-MHC
-bind to & display peptide fragments from self or non-self proteins (eg. degraded microbial proteins) on the cell surface for recognition by appropriate T cells
-invasion alert

82
Q

Major histocompatibility complex

A

-MHC
-bind to & display peptide fragments from self or non-self proteins (eg. degraded microbial proteins) on the cell surface for recognition by appropriate T cells
-invasion alert

83
Q

MHC I

A

Glycoproteins on all nucleated cells

Intrinsic - Tc (CD8) - kill infected cell with intracellular pathogen

84
Q

MHC II

A

Glycoproteins only on APCs

Extrinsic - Th (CD4) - help B cell make Ab to extracellular pathogen

85
Q

MHC III

A

Code for secreted proteins

86
Q

Cell mediated immunity

A

INTRACELLULAR

Interlay between

APCs (macrophages, dendritic cells, B cells)

and

T cells

-requires intimate cell to cell contact
-control Ab responses via contact with B cells
-directly recognise & kill viral infected cells

87
Q

What does cell-mediated immunity require?

A

MHC
Intrinsic (endogenous) antigens
Extrinsic (exogenous) antigens
Recognise self/non-self

88
Q

Humoral immunity

A

EXTRACELLULAR

89
Q

What type of Ag will T cells respond to?

A

Only respond to intracellular presented antigens

90
Q

B cell activation

A

-B cells become activated upon binding with an antigen - a specific B cell binds to a specific antigen - the right B cell has to be selected to bind - clonal selection
-then travel to the lymph nodes where clonal expansion takes place with the cells differentiating into plasma cells
-plasma cells secrete Ab (usually IgM)
-IgM later turn into IgG
-B cells divide - clonal expansion - differentiate into plasma cells & B memory cells
-re-stimulation of memory B cells lead to secondary response

91
Q

Which cells are APC?

A

Dendritic cells (primary APC)
Macrophages
B cells

92
Q

T cell selection

A

-T cells bearing autoreactive T cell antigen receptors (TCRs) are eliminated during the their development in the thymus (foetal)
-these are T cells that recognise self

92
Q

T cell selection

A

-T cells bearing autoreactive T cell antigen receptors (TCRs) are eliminated during the their development in the thymus (foetal)
-these are T cells that recognise self

2A CLINICAL SCIENCES (14 decks)

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