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MICR 386 Learning Outcomes > MODULE 5 - 9 > Flashcards

MODULE 5 - 9 Flashcards

1
Q

4 main attributes of cytokines

A

pleiotrophy, redundancy, synergy, antagonism

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2
Q

Pleiotrophy

A

a single cytokine can produce multiple effects

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3
Q

Example of Pleiotrophy

A

Il-4 stimulates multiple effects on B-cells

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4
Q

Redundancy

A

Cytokines can target the same cell and elicit the same effect

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5
Q

Example of redundancy

A

IL-2, IL-4, and IL-5 can stimulate B-cells to undergo proliferation

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6
Q

Synergy

A

the combined effect is greater than the added effect of them seperately

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7
Q

Example of synergy

A

IL-4 and IL-5 together can more effectively stimulate B-cells to induce class switching to IgE

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8
Q

Antagonism

A

cytokines can act on other cuytokines to impact their effects

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9
Q

Example of antagonism

A

IL-4 functions to induce B-cell class switching, but IFN-gamma can act to block the effects of IL-4

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10
Q

5 Cytokine receptor classes

A

Ig Superfamily Receptors, Class I Receptors, Class II Receptors, TNF Receptor Family, Chemokine Receptor Family

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11
Q

Ig Superfamily Receptors

A

has the same domain structure found on MHCs and Igs

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12
Q

Ig Superfamily Receptors Ligand

A

IL-1: induces fever through hypothalamus stimulation

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13
Q

Class I Receptors

A

have Trp-Ser-X-Trp-Ser (WSXWS) amino acid motif

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14
Q

Class I Receptors Ligand

A

IL-2, IL-3, pIL-4, IL-5, IL-6, IL-7, IL-12, IL-13

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15
Q

Class II Receptors

A

similar to Class I but don’t have WSXWS motif; has cys disulfide bonds

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16
Q

Class II Receptors Ligand

A

INF-alpha, INF-beta, INF-gamma, IL-10

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17
Q

TNF Receptor Family

A

have cys-rich domains

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18
Q

TNF Receptor Family Ligands

A

TNF-alpha, TNF-beta, CD40L, FAS

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19
Q

Chemokine Receptor Family

A

belong to G-protein coupled receptors; have 7 transmembrane domains

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20
Q

Chemokine Receptor Family Ligands

A

CCR5 and CXCR4: co-receptors for HIV

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21
Q

Th1 cells secrete

A

IFN-gamma: promotes TH1 differentiation, inhibits TH2 proliferation

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22
Q

Effector functions of Th1 cells

A

play role in the cell-mediated immune response

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23
Q

Th2 cells secrete

A

IL-4, IL-5, and a little IL-10: promotes Th2 differentiation, inhibits Th1 activation

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24
Q

Effector functions of Th2 cells

A

plays a role in the humoral immune response

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25
Q

Bacterial septic shock

A

gram-negative cell wall endotoxins stimulate the patients macrophages to over-produce IL-1 and TNF-alpha, leading to the secretion of additional pro-inflammatory cytokines (IL-6 and IL-8)

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26
Q

Symptoms of bactrial septic-shock

A

Macrophages secrete lipid mediators and reactive O2/N species, causing fever, diarrhea, organ dysfunction, and widespread clotting

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27
Q

Primary immune response on B-cells

A

activation and differentiation of naive B-cells into anti-body secreting plasma cells

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28
Q

Secondary immune response on B-cells

A

antigen-specific memory B-cells are preferentially activated, resulting in quick response

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29
Q

Primary immune response on Ig production

A

produces equal amounts of IgM and IgG over 4-7 days

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30
Q

Secondary immune response on Ig production

A

produces primarily IgG rapidly over 1-3 days and has an overall longer period of antibody concentration

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31
Q

T-cell dependent B-cell activation

A

When a helper T-cell recognizes an antigen:MHC class II complex on a B-cell, the T-cell becomes activated, which activates the B-cell

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32
Q

3 signals in T-cell Dependent B-cell Activation

A

TCR-MHC class II complex binding, costimulatory molecule signalling, cytokine signalling

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33
Q

TCR-MHC Class II Complex Binding

A
  1. Antigens are processed and presented to T-cells
  2. BCR binds its specific antigen resulting in internalization of the Ig-antigen complex by receptor-mediated endocytosis
  3. Antigen is then processed by the endocytic antigen processing pathway and is displayed on MHC class II molecules on cell surface
  4. TCR of the helper T-cell recognizes the processed Ag:MHC complex presented by the B-cell
  5. TCR and CD4 bind to the Ag:MHC class II complex, resulting in activation of the helper T-cell
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34
Q

Costimulatory molecule signalling

A
  1. Upon TCR recognition of the antigen, CD40L expression is induced on the surface of helper T-cell through TCR-mediated inositol lipid hydrolysis
  2. CD40L interacts with expressed CD40 on B-cell, CD40L-CD40 interaction activates cytokine receptor expression on cell surface of B-cell and T-cell
  3. MHC Class II mediated cAMP activation results in increased expression of B7 on the cell surface
  4. B7 binds CD28 expressed by T-cell and provides necessary costimulatory signal to activate the helper T-cell
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35
Q

Cytokine signalling

A
  1. B7-CD28 interaction induces the MAPK cascade in helper T-cell
  2. This cascade activates cJUN and cFos which form AP-1 transcription factor that activates IL-2 gene
  3. Cytokines bind their receptors on the B-cells and T-cells, initating proliferation and differentation
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36
Q

Type I T-cell independent antigens

A

polyclonal B-cell activators: capable of activating B-cell regardless of their antigenic specifity

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37
Q

Type 2 T-cell independent antigens

A

expressed on the surface of pathogens in an organized and highly repetitive form; can activate B-cells by cross-linking the membrane bound iG in a multivalent fashion

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38
Q

Type 2 T-cell independent antigens example

A

polymeric proteins or bacterial cell wall polysaccarides with repeating polysaccaride units

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39
Q

Effector cells

A

cells that have a biological effect rather

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40
Q

Effector cells in non-specific response

A

macrophages and NK cells

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41
Q

Results of non-specific response

A

increased IFN-alpha and IFN-beta, activate Th1 cell

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42
Q

Effector cells in specific response

A

Cytotoxic T-cells

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43
Q

Antigen-nonspecific response

A

Macrophages + NK cells can recognize pathogens, but are not specific to a particular antigen

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44
Q

Antigen-specific response

A

Th1 cells activate cytotoxic T-cells which are specific for a processed pathogen antigen in complex with MHC class I

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45
Q

The NK cell response is activated by:

A

IFN-alpha, IFN-beta, IL-2

46
Q

4 characteristics of the NK cell response:

A

1) These are large granular lymphocyte-like cells that lack antigen-specific receptors
2) They’re capable of Fas-mediating killing
3) They control infection during the period required for generation of specific cell-mediated effector cells
4) They’re involved in antibody-dependent cell mediated cytotoxicity

47
Q

Receptors on NK cells:

A

Killer inhibitory receptors (KIRs) recognize self MHC class I

48
Q

How do KIRs work

A

All normal cells have MHC class I molecules, but virally infected cells have downregulating expression of MHC class I molecules, so KIRs are not engaged and NK cells then kill the cell

49
Q

Antibody opsonization in ADCC

A

infected target cells express antigens, which are then marked to be phagocytosed

50
Q

Fc-gamma-RIII in ADCC

A

Receptors on NK cells recognized and bind the Fc portion of antibodies; once bound to an antibody:target cell, the NK cell is activated

51
Q

Activated NK cells in ADCC

A

activated NK cells bound to a target release the content of their cytolytic granules by directly killing the target cell or inducing FasL/Fas-mediated apoptosis

52
Q

Cytotoxic T-cell killing adhesion

A

LFA-1 and ICAM-1 interaction

53
Q

Cytotoxic T-cell killing antigen recognition

A

TCR:peptide/MHC complex binding

54
Q

Cytotoxic T-cell killing movement of granules

A

reorientation of cytoskeleton and cytoplasmic components

55
Q

Cytotoxic T-cell killing of target cell

A

“lethal hit,” pore formation, cell apoptosis

56
Q

3 complement pathways

A

Classical, alternative, lectin

57
Q

Classical pathway is activated by

A

immune complexes (Ag-Ab) involving human Igs IgM, IgG1, IgG2, and IgG3

58
Q

Alternative pathway is activated by:

A

Non-Ab substances such as lipopolysaccarides, polymers or venom factors

59
Q

Lectin-pathway is activated by

A

mannan, which is expressed only on bacteria and viruses

60
Q

7 steps of classical pathway

A

1) Antibodies bind to multivalent antigen on the cell membrane of the target cell; the C1 complex (C1qr2s2) binds the FC region of the antibody bound to the target cell
2) C4 then binds to the C1q portion of the Ig:C1 complex; r2s2 enyme cleaves C4 into C4a and C4b
3) C4b covalently attaches to the cell membrane or antibody; C2 binds to C4b; C1qr2s2 cleaves C2 into C2a and C2b
4) C4b and C2a combine to form C3 convertase (C4bC2a)
5) C3 convertase binds and cleaves C3 into C3a and C3b
6) C3b binds C4bC2a to form C5 convertase (C4bC2aC3b); C3a is hydrolyzed or bonds with target cell surfaces
7) C5 convertase binds to C5 and cleaves it into C5b

61
Q

8 step of lectin pathway

A

1) Serum mannose-binding lectin binds to mannose residues on glycoproteins or carbohydrates on surface of microbes; mannose-binding lectin is an acute phase protein produced during inflammation
2) Mannose-binding lectin-associated serine protease (MASP) binds to mannose-binding lectin (MBL)
3) The active MASP-MBL complex cleaves inactive C4 into active C4a and C4b
4) C4b can attach to pathogen cell via mannose binding; C2 binds C4b
5) C2 of the C4bC2 complex is cleaved by MASP to form C4bC2a (C3 convertase)
6) C3 convertase binds and cleave C3 into C3a and C3b
7) C3b binds to C4bC2a to form C5 convertase; C3a is hydrolyzed or bonds with target cell surfaces
8) C5 convertase binds to C5 and cleaves it into C5b

62
Q

7 steps of alternative pathway

A

1) Continuous cleavage of C3 occurs in plasma, resulting in C3a and C3b
2) C3b binds to microbial surface via active thioester bonds; factor B binds C3b
3) Factor D cleaves Factor B (still bound to C3b)
4) Factor P stabilizes C3bBb, making it C3 convertase
5) Cleavage of another C3 by cell-associated C3bBb, giving C3a and C3b
6) C3b binds to the cell surface, forming C3bBbC3b complex (C5 convertase)
7) C5 convertase cleave C5 into C5b

63
Q

Mnuemonic to remember Classical, Alternative, and Lectin Pathways

A

Classroom 142, Lecture 42, Focused on Classical or Developmental Biology

64
Q

C1, C2, C4 Deficiency

A

Immune complex disease

65
Q

C3, Factor D, Factor I Deficiency

A

Pyogenic infections

66
Q

MBL deficiency

A

susceptible to reccurent infections and decrease lung function in cystic fibrosis patients

67
Q

4 steps of complememnt cascade after C5 convertase formation

A

1) Cell-associated C5 convertase cleaves C5 into C5a and C5b; C5b remains bound to C5 convertase
2) C6 and C7 sequentially bind to C5b; C5bC6C7 complex becomes directly inserted into the lipid bilayer of the target cell membrane
3) C8 is bound to C7 to stabilize the complex
4) Up to 15 C9 molecules polymerize around the C5bC6C7C8 complex to form the membrane attack complex (MAC)

68
Q

Type 1 Gell-Coombs Hypersensitivity Reactions

A

Specific antibody-mediated reaction that can develop into anaphylactic responses

69
Q

Type 1 Gell-Coombs Hypersensitivity Reactions occur due to

A

IgE on mast cell binds an allergen, resulting in mast cell degranulation C3a, C4a, and C5a can also cause this reaction

70
Q

4 typical Type 1 Gell-Coombs Hypersensitivity Reaction Allergens

A

Fel d1 and Fel4 (cats), Fra a1 (strawberries), hyaluronidase (honeybee venom), Der p1 (Dust mite feces)

71
Q

Mechanism of Type 1 Gell-Coombs Hypersensitivity Reactions

A

Ag induces cross-linking of IgE mast cells with release of vasoactive mediators

72
Q

Clinical manifestations of Type 1 Gell-Coombs Hypersensitivity Reactions

A

Atopy, asthma, laryngeal edema

73
Q

Type 2 Gell-Coombs Hypersensitivity Reactions

A

mediated by an antibody directed against cell surface antigens

74
Q

What results from Type 2 Gell-Coombs Hypersensitivity Reactions

A

Hemolytic anemia, bullous pemphigus, transfusion reactions, Rh disease

75
Q

Type 3 Gell-Coombs Hypersensitivity Reactions

A

mediated by an Ab-Ag immune complex deposited on the tissue

76
Q

What results from Type 3 Gell-Coombs Hypersensitivity Reactions

A

Immune complexes activate complement and recruit innate cells to cause tissue damage

77
Q

Mechanism of Type 3 Gell-Coombs Hypersensitivity Reactions

A

Ag-Ab complexes deposited in various tissues induce complement activation and an ensuing inflammatory response mediated by massive infiltration of neutrophils

78
Q

Clinical presentation of Type 3 Gell-Coombs Hypersensitivity Reactions

A

Serum sickness, farmer’s lung, rheumatoid arthritis

79
Q

Type 4 Gell-Coombs Hypersensitivity Reactions

A

Involves a complex intervention of T-cells and monocytes/macrophages

80
Q

Mechanism for Type 4 Gell-Coombs Hypersensitivity Reactions

A

Sensitized T-cells release inflammatory cytokines that activate macrophages which mediate direct cellular damage

81
Q

Mechanism for Type 2 Gell-Coombs Hypersensitivity Reactions

A

Ab directed against cell surface antigens mediates cell destruction via complememnt activation or ADCC

82
Q

Clinical presentation for Type 4 Gell-Coombs Hypersensitivity Reactions

A

conact dermatitis, tubercular lesion, gluten intolerance

83
Q

Atopy

A

exaggerated IgE-mediated immune response to environmental allergen

84
Q

Asthma

A

inflamation and obstructed airways that can be both atopic and non-atopic

85
Q

Laryngeal edema

A

swelling of the larynx with high pitch breathing sound

86
Q

Hemolytic anemia

A

condition where immune system recognizes own RBCs as foreign

87
Q

Bullous pemphigus

A

autoimmune skin disease resulting in formation of blisters between epidermis and dermis

88
Q

Transfusion reactions

A

Adverse reaction to allogenic RBCs following transfusion reaction

89
Q

Rh disease

A

hemolytic condition where maternal and fetal blood are not compatible

90
Q

Serum sickness

A

Reaction to proteins in antiserum derived from non-human animals

91
Q

Farmer’s lung

A

Hypersensitivity pneumonitis

92
Q

Rheumatoid arthritis

A

long-term autoimmune disorder involving both Type 1 and Type 2 hypersensitivity

93
Q

Contact dermatitis

A

a reactive chemical binds to skin proteins and presented to T-cells

94
Q

Gluten intolerance

A

Reaction to giladen antigen causing atrophy in small bowel

95
Q

Central tolerance

A

Mechanism where immune system learns to discriminate self vs non-self antigens

96
Q

Peripheral tolerance

A

mechanism where the body prevents over-reactivity to environmental factors

97
Q

Autoimmune disease have been linked to

A

certain MHC haplotypes - as they may fail to delete anti-self T-cells or B-cells

98
Q

Sympathetic Uveitis

A

Inflammation that occurs following insult to the eye

99
Q

Clinical presentation of sympathetic uveitis

A

mutton-fat keratic precipitates, choroidal infiltrations, Dalen-Fuchs nodules

100
Q

Myathenia gravis

A

antibodies against nicotinic Ach receptors at neuromuscular joint prevent Ach from binding, preventing muscle contractions

101
Q

Clinical presentation myathenia gravis

A

muscle weakness, drooping eyelids (ptosis)

102
Q

Grave’s disease

A

manifests as hyperthyroidism due to antibodies against TSH receptor

103
Q

Clinical presentation of Grave’s disease

A

goitre-swelling of neck from enlarged thyroid gland, bulging eyes

104
Q

Organ-specific autoimmune disease

A

immune response against self antigen of a single organ

105
Q

Systemic autoimmune disease

A

immune response against self-antigens throughout many tissues

106
Q

Primary immunodeficiency

A

genetic defects result in absence of functioning immune system parts

107
Q

Secondary immunodeficiency

A

environmental factors that compromise the immune system

108
Q

4 factors of secondary immunedeficiency

A

malnutrition, medication, aging, disease

109
Q

Malnutrition

A

protein deficiency leads to a decreased ability to fight infection

110
Q

Medication

A

Cytotoxic agents target rapidly dividing cells which supress the immune system

111
Q

Aging

A

Thymus shrinks, producing fewer T-cells

MICR 386 Learning Outcomes (1 decks)

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