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Flashcards in Immune response Deck (104):
1

Acute phase reactants - definition

Factors whose concentrations change significantly in response to inflammation

2

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

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

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Acute phase reactants - types and the way that they change

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

4

C-reactive protein - function and clinical relevance

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

5

Ferritin - function (as an acute phase reactant)

Binds and sequesters iron to inhibit microbial iron scavenging

6

Fibrinogen - function (as an acute phase reactant)

1. coagulation factor
2. promotes endothelial repatir

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Hepcidin - function

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

8

Acute phase reactants - serum amyloid A?

prolonged elevation --> amyloidosis

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Acute phase reactants - albumin

reduction conserves aminoacids for positive reactants

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Acute phase reactants - transferrin

internalized by macrophages to sequester iron

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

liver / role in innate immunity and inflammation

12

Membrane attach complex (MAC) defends against

Gram (-) bacteria

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Complement activation - pathways (generally mediated by)

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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complement function (and which types)

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

15

primary opsonins in bacterial defence

1. C3b
2. IgG

16

beside phagocytosis enhancement , C3b also help

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

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Complement inhibitos

1. Decay-accelerating factor (DAF, aka CD55)
2. C1 esterase inhibitor help prevent complement activation on self cells (eg. RBCs)

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Decay-accelerating factor (DAF) is aka

CD55

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complement activation - alternative pathway

- 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

20

complement activation - classic pathway

- 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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complement activation - lectin pathway

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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C2 historically

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

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Complement disorders - types

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

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C1 esterase inhibitor deficiency?

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

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contraindicated in C1 esterase inhibitor deficiency? (why)

ACE inhibitors
because ACE inhibits bradykinin

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C3 deficiency?

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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C5-9 deficiency?

Terminal complement deficiency increases susceptibility to recurrent Neisseria bacteremia

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DAF (GPI-anchored enzyme) deficiency

Causes complement-mediated lysis of RBCs and paroxysmal noctural hemoglobinuria

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Important cytokines secreted by macrophages

IL-1, 6, 8, 12, TNFa

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Important cytokines secreted by ALL T cells

IL-2, IL-3

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Important cytokines secreted from Th1 cells

Interferon γ

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Important cytokines secreted from Th2 cells

IL-4, 5, 10, 13

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IL-1 is AKA

osteoclast-activating factor

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IL-1 causes

1. fever
2. acute inlammation
3. Cachexia

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IL-1 causes acute inflammation - mechanism

1. acivates endothelium to express adhesion molecules
2. induce chemokine secretion to recroit WBCs

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IL-6 -->

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

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IL-8 -->

major chemotactic factor for neutrophils

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IL-12 -->

1. induce differentiation of T cells into Th1 cells
2. Activates NK cells

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TNF-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

40

IL-2 -->

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

41

IL-3 -->

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

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INF-γ is secreted by

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

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INF-γ -->

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

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IL-4 -->

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

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IL-5 -->

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

46

IL-10 -->

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

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beside Th2 cells, il-10 is also secreted by

T reg cells

48

cytokines that attenuate the immune response

1. TGF-β
2. IL-10

49

Respiratory burst is AKA, and definition

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

50

Respiratory burst (oxidative burst) plays important role in

immune response --> rapid release of ROS

51

ROS - pathway

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

glutatione pathway

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)

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NADPH oxidase deficiency

chronic granulomatous disease

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Patients with chronic granulomatous disease -->

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

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Pyocyanin of P. aeruginosa - function

generate ROS to kill competing microbes

56

Lactoferrrin is a

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

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NAPDH - role in ROS

it plays a role in both creation and neutraliation of ROS

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Myeloperoxidase - function and appearance

H20 + CL- --> HCLO3 (Myeloperoxidase) --> destroys bacteria
blue green heme-containing pigment that gives sputum its color

59

Interferons structure

glycoproteins

60

Interferons -a - β function

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

61

Interferons are glycoproteins synthesizes by (and function)

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

interferons as drugs - clinical use

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

interferons as drugs - side effects

1. neutropenia
2. myopathy
3. depression
4. flu-like

64

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

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

65

Cell surface proteins - specific for T helper

CD4
CD40L

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Cell surface proteins - specific for Cytotoxic T cell

CD8

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Cell surface proteins - reg T cells

CD4
CD25

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Cell surface proteins - B cells

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

69

receptor of EBV in B cells

CD21

70

Cell surface proteins - NK cells (and characteristics)

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

71

Cell surface proteins - hematopoetic stem cells

CD34

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Cell surface proteins - Macrophages

CD14, CD40, CCR5, MHCII,
B7 (CD80/86), Fc and C3b receptos

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Macrophage - function of CD14

receptor for PAMPS
co-receptor of Toll-like receptor

74

Anergy?

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

75

T and B cells anergy

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

76

Superantigens are produced by

1. S. aureus (TSST-1)
2. S. pyogenes (exotoxin A)

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superantigens action

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

endotoxins/LPS acion

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

79

examples of antigenic variation

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

80

antigenic variation - mechanism

some mechanism for variation include DNA rearrangementt and RNA segment reassortment

81

Passive vs active immunity according to mechanism of acquisition and onset

Passive --> receiving preformed antibodies --> rapid
Active --> Exposure to foreign antigens --> slow

82

Passive vs active immunity according to duration

Passive --> short span of antibodies (hald-life = 3 weeks)
Active --> long lasting protection (memory)

83

Passive immunity - example (4)

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

84

Active immunity - examples (3)

1. Natural infection
2. Vaccines
3. Toxoid

85

combined passive and active immunization can be given for

hepatitis B or rabies exposure

86

humanized monoclonal antibody - definition

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

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

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

88

Vaccination induces

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

89

Viral vaccines - categories and viruses

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))

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Life attenuated vaccine - description

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

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inactivated or killed vaccine - description

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

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

Life attenuated --> cellular and humoral responses
Inactivated or killed --> humoral response

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Life attenuated vaccine - pros and con

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

94

Life attenuated vaccine is often contraindicated in

pregnancy and immunodeficiency

95

Life attenuated vaccine - HIV

MMR and VZV if cd more than 2 hundred

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inactivated or killed vaccine - pros and con

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

97

Fibrinogen correlates with

ESR

98

B7 is aka (and is found at)

CD 80/86
B cells and macrophages

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CD 40 is found in

B cells and macrophages

100

LPS binds to (receptor)

TLR4/CD14

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live attenuated vaccine but not for virus

BCG
salmonella typhi

102

CD55?

DAF

103

BCG developed from

Mycobacterium bovis

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influenza vaccine

1. live --> intranasal
2. killed --> injected