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Immunology > Immune response > Flashcards

Immune response Flashcards

1
Q

Acute phase reactants - definition

A

Factors whose concentrations change significantly in response to inflammation

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2
Q

Acute phase reactants produced by (when, and induced by)

A

produced by liver in both acute and chronic inflammatory states
Notably induced by Il-6

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3
Q

Acute phase reactants - types and the way that they change

A

upregulated: 1. C-reactive protein 2. Ferretin 3. Fibrinogen 4. Hepcidin 5. Serum amyloid A down
downregulated: 1. albumin 2. transferrin

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4
Q

C-reactive protein - function and clinical relevance

A
  1. opsonin (enhances phagocytosis)
  2. Fixes complement
    - -> Measured clinically as a sign of ongoing inflammation
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5
Q

Ferritin - function (as an acute phase reactant)

A

Binds and sequesters iron to inhibit microbial iron scavenging

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6
Q

Fibrinogen - function (as an acute phase reactant)

A
  1. coagulation factor

2. promotes endothelial repatir

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7
Q

Hepcidin - function

A

decreases iron absorption (by degrading ferroportin) and decreases iron release (from macrophages) –> anemia of chronic disease

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8
Q

Acute phase reactants - serum amyloid A?

A

prolonged elevation –> amyloidosis

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9
Q

Acute phase reactants - albumin

A

reduction conserves aminoacids for positive reactants

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10
Q

Acute phase reactants - transferrin

A

internalized by macrophages to sequester iron

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11
Q

Complement is produced by …/ play role in …. (generally)

A

liver / role in innate immunity and inflammation

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12
Q

Membrane attach complex (MAC) defends against

A

Gram (-) bacteria

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13
Q

Complement activation - pathways (generally mediated by)

A
  1. classic pathway - IgG or IgM mediated
  2. Alternative pathway - microbe surface molecules and spontaneous
  3. Lectin pathway - mannose or other sugars on microbe surface
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14
Q

complement function (and which types)

A
  1. oponization: C3b
  2. anaphylaxis: C3a, C4a, C5a
  3. neutrophil chemotaxis: C5a
  4. cytolyisis by MAC: C5b-9
  5. helps cliar immune complex: C3b
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15
Q

primary opsonins in bacterial defence

A
  1. C3b

2. IgG

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16
Q

beside phagocytosis enhancement , C3b also help

A

clear immune complexes (C3b-tagged immune complex is destroyed)

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17
Q

Complement inhibitos

A
  1. Decay-accelerating factor (DAF, aka CD55)

2. C1 esterase inhibitor help prevent complement activation on self cells (eg. RBCs)

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18
Q

Decay-accelerating factor (DAF) is aka

A

CD55

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19
Q

complement activation - alternative pathway

A
  • C3 + spontantenous/microbial surface –> C3b
  • C3b + Bp factor (B+D–>Bd) –> C3Bd convertase
  • C3bBd (C3 convertase) + C3 –> C3a + C3b
  • C3b + C3bBd –> C3bBd3b (C5 convertase)
  • C3bBd3b + C5 –> C5a + C5b
  • C5b + C6-9 –> mac –> lysis, cytotoxicity
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20
Q

complement activation - classic pathway

A
  • C1 + antigen-antibody complex (IgM, IgG) –> activate C1
  • activated C1 + C4 + C2 –> C4a + C4b + C2a + C2b
  • C4b + C2b –> C4b2b (C3 convertase)
  • C3b + C4b2b –> C4b2b3b (C5 convertase)
  • C4b2b3b + C5 –> C5a + C5b
  • C5b + C6-9 –> mac –> lysis, cytotoxicity
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21
Q

complement activation - lectin pathway

A

C1 + Microbial surface (eg. maltose) –> C1 like complex (activated C1)

  • activated C1 + C4 + C2 –> C4a + C4b + C2a + C2b
  • C4b + C2b –> C4b2b (C3 convertase)
  • C3b + C4b2b –> C4b2b3b (C5 convertase)
  • C4b2b3b + C5 –> C5a + C5b
  • C5b + C6-9 –> mac –> lysis, cytotoxicity
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22
Q

C2 historically

A

the larger fragment of of C2 was called C2a but is now referred to as C2b

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23
Q

Complement disorders - types

A
  1. C1 esterase inhibitor deficiency
  2. C3 deficiency
  3. C5-9 deficiency
  4. DAF (GPI-anchored enzyme) deficiency
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24
Q

C1 esterase inhibitor deficiency?

A

causes hereditary angioedema due to upregulated activation of kallikerein –> increased bradykinin –> VASODILATION, PERMEABILITY, INCREASES PAIN

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25
Q

contraindicated in C1 esterase inhibitor deficiency? (why)

A

ACE inhibitors

because ACE inhibits bradykinin

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26
Q

C3 deficiency?

A
  1. increases risk of severe, recurrent pyogenic sinus and respiratory tract infection
  2. increased susceptibility to type III hypersensitivity reaction (C3b helps to clear ICs)
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27
Q

C5-9 deficiency?

A

Terminal complement deficiency increases susceptibility to recurrent Neisseria bacteremia

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28
Q

DAF (GPI-anchored enzyme) deficiency

A

Causes complement-mediated lysis of RBCs and paroxysmal noctural hemoglobinuria

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29
Q

Important cytokines secreted by macrophages

A

IL-1, 6, 8, 12, TNFa

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30
Q

Important cytokines secreted by ALL T cells

A

IL-2, IL-3

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31
Q

Important cytokines secreted from Th1 cells

A

Interferon γ

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32
Q

Important cytokines secreted from Th2 cells

A

IL-4, 5, 10, 13

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33
Q

IL-1 is AKA

A

osteoclast-activating factor

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34
Q

IL-1 causes

A
  1. fever
  2. acute inlammation
  3. Cachexia
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35
Q

IL-1 causes acute inflammation - mechanism

A
  1. acivates endothelium to express adhesion molecules

2. induce chemokine secretion to recroit WBCs

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36
Q

IL-6 –>

A
  1. fever
  2. stimulates production of acute-phase proteins
  3. Cachexia
  4. Th –> Th17 (with il-6)
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37
Q

IL-8 –>

A

major chemotactic factor for neutrophils

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38
Q

IL-12 –>

A
  1. induce differentiation of T cells into Th1 cells

2. Activates NK cells

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39
Q

TNF-a –>

A
  1. mediates septic shock
  2. Cachexia in malignancy
  3. acute inflammation (WBC recruitment, activates endothelium, vascular leak)
  4. Apoptosis (instrict pathway)
  5. induce and maintains granuloma formation
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40
Q

IL-2 –>

A

stimulates growth of helper, cytotoxic and regulatory T cells and NK cells

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41
Q

IL-3 –>

A

supports growth and differentiateion of bone marrow stem cells (function like GM-CSF)

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42
Q

INF-γ is secreted by

A

NK cells and T cells in response to il-12 from macrophages

43
Q

INF-γ –>

A
  1. stimulates macrophages to kill phagocytosed pathogens
  2. Inhibits differentiation of Th2
  3. activates NK cells to kill virus infected-cells
  4. increases MHC expression and antigen presentation by all cells
44
Q

IL-4 –>

A
  1. induce differentation of T cells into Th2
  2. Promotes growth of B cells
  3. Inhibit Th1 differentiation
  4. Enhance class switching to IgE and IgG
45
Q

IL-5 –>

A
  1. Promotes growth and differentation of B cells
  2. Enhance class switching to IgA
  3. Stimulates growth and differentiation of eosinophils
46
Q

IL-10 –>

A
  1. attenuates inflammatory response
  2. decreases expression of MHC II and Th1 cytokines
  3. Inhibits activaed macrophages and dendritic cells
  4. Inhibit differentiation of Th to Th1
47
Q

beside Th2 cells, il-10 is also secreted by

A

T reg cells

48
Q

cytokines that attenuate the immune response

A
  1. TGF-β

2. IL-10

49
Q

Respiratory burst is AKA, and definition

A

oxidative burst

is the rapid release of ROS from different types of cells.

50
Q

Respiratory burst (oxidative burst) plays important role in

A

immune response –> rapid release of ROS

51
Q

ROS - pathway

A

O2 + NADPH –> 02- + NADP+ (NADPH oxidase)
02- –> H202 (Superoxide dismutase)
H20 –> a. H20 + 02 (bacterial catalase)
b.H20 + CL- –> HCLO (Myeloperoxidase) –> destroys bacteria
c. glutathione pathway
02–>superoxide anion
HCLO–>Bleach (Hypochlorite)
H202–>Hydrogen peroxide

52
Q

glutatione pathway

A

NADP+ + Glucose-6-P –> NADPH + 6-phosphpgluconate
(G6PD)
NADPH + oxidazed Glutathione –> NADP+ + reduced glutathione (Glutathione reductase)
REDUCED GLUTATHIONE destroys H202
reduced glutathione + H202 –> oxidazed Glutathione + H2O (Glutathione peroxide)
Glutathione enzymes (peroxidase and reductase requires selinium)

53
Q

NADPH oxidase deficiency

A

chronic granulomatous disease

54
Q

Patients with chronic granulomatous disease –>

A

can untlize H2O2 by invading organisms and convert it to ROS. High risk at CAT+ species capable of neutralizing their own H2O2, leaving phagocytes without ROS for fiighting infections

55
Q

Pyocyanin of P. aeruginosa - function

A

generate ROS to kill competing microbes

56
Q

Lactoferrrin is a

A

protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation

57
Q

NAPDH - role in ROS

A

it plays a role in both creation and neutraliation of ROS

58
Q

Myeloperoxidase - function and appearance

A

H20 + CL- –> HCLO3 (Myeloperoxidase) –> destroys bacteria

blue green heme-containing pigment that gives sputum its color

59
Q

Interferons structure

A

glycoproteins

60
Q

Interferons -a - β function

A

a part of innate host defense against both RNA + DNA viruses

61
Q

Interferons are glycoproteins synthesizes by (and function)

A

virus infected cells that act locally on unifected cells priming them for viral defense by helping to selectively degrade viral nuclei acid and protein

62
Q

interferons as drugs - clinical use

A

Interferons - α: 1. chronic hepatitis B, C 2. Kaposi sarcoma 3. hairy cell leukemia 4. condyloma acuminatum 5. renal cell carcinoma 6. malignant melanoma
Interferons - β: multiple sclerosis
Interferons - γ: chronic granulomatous disease

63
Q

interferons as drugs - side effects

A
  1. neutropenia
  2. myopathy
  3. depression
  4. flu-like
64
Q

Cell surface proteins - T cells (and briefly their function)

A

TCR (binfs antigen-MHC complex)
CD3 (associated with TCR for signal transduction
CD28 (binds B7 on APC)
CXCR4/CCR5 (co-receptor for HIV)

65
Q

Cell surface proteins - specific for T helper

A

CD4

CD40L

66
Q

Cell surface proteins - specific for Cytotoxic T cell

A

CD8

67
Q

Cell surface proteins - reg T cells

A

CD4

CD25

68
Q

Cell surface proteins - B cells

A

Ig , CD 19, CD20, CD21, CD40, MHC II, B7

69
Q

receptor of EBV in B cells

A

CD21

70
Q

Cell surface proteins - NK cells (and characteristics)

A

CD16 –> binds FC of IgG –> antibody dependent cell-mediated cytotoxicity
CD56 –> unique marker for NK cells

71
Q

Cell surface proteins - hematopoetic stem cells

A

CD34

72
Q

Cell surface proteins - Macrophages

A

CD14, CD40, CCR5, MHCII,

B7 (CD80/86), Fc and C3b receptos

73
Q

Macrophage - function of CD14

A

receptor for PAMPS

co-receptor of Toll-like receptor

74
Q

Anergy?

A

state during which a cell cannot became activated by exposure to its antigen

75
Q

T and B cells anergy

A

when exposed to their antigen without constimulatory signal (signal 2). Another mechanism of self-tolerence

76
Q

Superantigens are produced by

A
  1. S. aureus (TSST-1)

2. S. pyogenes (exotoxin A)

77
Q

superantigens action

A

cross link the β region of the T-cell receptor to the MHC II on APC –> can activate any CD4+ T cell –> massive release of cytokines

78
Q

endotoxins/LPS acion

A

directly stimulate macrophage by binding to endotoxin receptor TLR4/CD14
Th cells are not involved

79
Q

examples of antigenic variation

A

Parasites - trypanosomes (reccuring fever)
Viruses - influenza, HIV, HCV
Bacteria: a. Salmonella (2 flagerllar variants), Borrelia recurrentis (relapsing fever), N. gonorrhoeae (pilus protein)

80
Q

antigenic variation - mechanism

A

some mechanism for variation include DNA rearrangementt and RNA segment reassortment

81
Q

Passive vs active immunity according to mechanism of acquisition and onset

A

Passive –> receiving preformed antibodies –> rapid

Active –> Exposure to foreign antigens –> slow

82
Q

Passive vs active immunity according to duration

A

Passive –> short span of antibodies (hald-life = 3 weeks)

Active –> long lasting protection (memory)

83
Q

Passive immunity - example (4)

A
  1. IgA in breast milk
  2. maternal IgG crossing placenta
  3. antitoxin
  4. humanized monoclonal antibody
84
Q

Active immunity - examples (3)

A
  1. Natural infection
  2. Vaccines
  3. Toxoid
85
Q

combined passive and active immunization can be given for

A

hepatitis B or rabies exposure

86
Q

humanized monoclonal antibody - definition

A

combined human antibody with a small part of a mouse monoclonal antibody. The mouse part binds the antigen and the human part makes it less likely to be destroyed by the body’s immune system.

87
Q

unvaccinated patients are given preformed antibodies (passive) after exposure to

A
  1. Tetanus toxin
  2. Botulinum toxin
  3. HBV (both passive and active)
  4. Varicella
  5. Rabies
88
Q

Vaccination induces

A

an active immune response (humoral/or cellular) to specific antigens

89
Q

Viral vaccines - categories and viruses

A

A. Live attenuated vaccines (1. smallpox 2. yellow fever 3. rotavirus 4. VZV 5. Sabin polio 6. Influenza (intransal) 7. Measles 8. Mumps 9. Rubella)
B. Killed (1. Rabies 2. Influenza (injected) 3. Salk Polio 4. HAV)
C. Subunit (1. HBV (antigen=HBsAg) 2. HPV (types 6, 11, 16, 18))

90
Q

Life attenuated vaccine - description

A

Microorganism loses its pathogenicity but retains capacity for transient growth within inoculated host –> induces cellular and humoral responses

91
Q

inactivated or killed vaccine - description

A

Pathogen is inactivated by heat or chemicals –> maintaining epitope structure on surface antigens is important for immune response –> mainly induces a humoral response

92
Q

Life attenuated vaccine vs inactivated or killed vaccine according to immune response

A

Life attenuated –> cellular and humoral responses

Inactivated or killed –> humoral response

93
Q

Life attenuated vaccine - pros and con

A

Pros: induce strong, often lifelong immunity
Con: may revert to virulent form

94
Q

Life attenuated vaccine is often contraindicated in

A

pregnancy and immunodeficiency

95
Q

Life attenuated vaccine - HIV

A

MMR and VZV if cd more than 2 hundred

96
Q

inactivated or killed vaccine - pros and con

A

Pro: safer than live vaccine
Con: weaker immune response (booster shot usually required)

97
Q

Fibrinogen correlates with

A

ESR

98
Q

B7 is aka (and is found at)

A

CD 80/86

B cells and macrophages

99
Q

CD 40 is found in

A

B cells and macrophages

100
Q

LPS binds to (receptor)

A

TLR4/CD14

101
Q

live attenuated vaccine but not for virus

A

BCG

salmonella typhi

102
Q

CD55?

A

DAF

103
Q

BCG developed from

A

Mycobacterium bovis

104
Q

influenza vaccine

A
  1. live –> intranasal

2. killed –> injected

Immunology (10 decks)

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