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IHO Ben > Week 1: Innate Immunity > Flashcards

Week 1: Innate Immunity Flashcards

1
Q

What are major functions of innate immunity?

A

Complement activation, Inflammation, cell activation, priming of the adaptive immune response

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2
Q

What does the innate immune system recognize?

A

Foreign molecular structures called pathogen-associated molecular patterns (PAMPs), stress or damage indicators expressed by body cells (DAMPs), The absence of certain “self” marker molecules

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3
Q

What PAMPS does TLR1 recognize?

A

Triacyllipopeptides

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4
Q

What PAMPS does TLR2 recognize?

A

Peptidoglycans, GPI-linked proteins, lipoproteins, zymosan, phosphatidylserine

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5
Q

What PAMPS does TLR3 recognize?

A

dsRNA

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6
Q

What PAMPS does TLR4 recognize?

A

LPS, F-protein, mannans

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7
Q

What PAMPS does TLR5 recognize?

A

Flagellin

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8
Q

What PAMPS does TLR6 recognize?

A

diacyllipopolypeptides, zymosan

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9
Q

What PAMPS does TLR7 recognize?

A

ssRNA

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10
Q

What PAMPS does TLR8 recognize?

A

ssRNA

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11
Q

What PAMPS does TLR9 recognize?

A

CpG unmethylated dinucleotides, dinucleosides, HSV components, Hemozoin

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12
Q

What happens when a TLR recognizes a PAMP?

A

It triggers cell signaling leading to gene transcription events to combat the foreign material

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13
Q

What PAMPs do C-type lectin receptors recognize?

A

mannose receptor, Dectin 1, DC-SIGN

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14
Q

What PAMPS does scavenger receptors recognize?

A

SR-A, SR-B

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15
Q

What occurs when either a C-type lectin receptor or a scavenger receptor recognize a PAMP?

A

They initiate phagocytosis

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16
Q

What kinds of chemicals are involved when a cell phagocytizes a bactera?

A

Reactive oxygen/nitrogen species

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17
Q

What is the overall goal of the complement system?

A

control inflammation

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18
Q

What is involved in the alternative pathway of the complement system?

A

opsonization and facilitated uptake of coated microorganism by phagocytes

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19
Q

What is involved in the classical pathway of the complement system?

A

Opsonization, chemotaxis of phagocytes, increased blood flow, increased permeability and damage to plasma membranes on cells of invader, release of inflamm. mediator from mast cells

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20
Q

Is the classical pathway a part of the adaptive or innate immune system?

A

adaptive

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21
Q

Is the lectin and alternative pathways a part of the innate or adaptive immune system?

A

Innate

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22
Q

What proteins are involved in the classical pathway of complement?

A

C1q (cleaves and initiates downstream complement compounds) and C5b (binds to membrane and forms the membrane attack complex)

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23
Q

What proteins are involved in the lectin pathway?

A

Mannose binding protein (binds to bacterial carbohydrates and initiates downstream complement compounds), C5b (membrane attack complex)

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24
Q

What proteins are involved in the alternative pathway?

A

C3 (spontaneously cleaved by serum proteases activated by bacteria), C3b (leads to downstream activation of complement components)

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25
Q

T/F: antigen-antibody complexes activate the classical pathway?

A

True

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26
Q

T/F: microorganisms activate the lectin pathway

A

True

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27
Q

T/F: Microorganisms activate the alternative pathway

A

True

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28
Q

What is the function of C3a, C4a and C5a?

A

chemotactic factors that increase directional migration of PMNs and macrophages, activate PMNs, macrophages, mast cells and basophil degranulation, ca

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29
Q

In terms of potency, describe which is more powerful: C3a, C4a and C5a

A

C5a&raquo_space;> C3a&raquo_space;> C4a

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30
Q

What is the function of C3b and C4b?

A

deposited on any surface with an exposed amine or hydroxyl, acting as opsonins, cleave more C3

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31
Q

What prevents opsonization of host cells?

A

decay-accelerating factor (DAF) for C3b and C4b, protectin (CD59) and homologous restriction factor (HRF) for C5b

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32
Q

What is the function of C5b?

A

binds to microorganisms or host body cells, acts as a focal point for the deposition of the membrane attack complex

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33
Q

What opsonin receptors lead to phagocytosis?

A

Collagen-domain receptor (CD91/calreticulin), Complement receptors (CR1, CR3, CR4, CRIg, C1qRp), Ig Fc receptors (Fc(alpha)R, Fc(gamma)R)

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34
Q

What are the four hallmarks of inflammation?

A

Influx of fluid (edema), Increased temp (hyperthermia), Decreased oxygenation (local hypoxia), Influx of WBCs (extravasation)

35
Q

What complement protein stimulates basophils and mast cells to degranulate?

A

C5a

36
Q

What is the result of histamine release?

A

increased vascular permeability

37
Q

What is the result of Prostaglandin E2 release?

A

vasodilation, increased vascular permeability

38
Q

What is the result of Leukotriene D2 release?

A

neutrophil chemotaxis, increased vascular permeability

39
Q

What is the result of leukotriene D4 released?

A

increased vascular permeability

40
Q

What is released as a result of mast cell and basophil degranulation?

A

Histamine, prostaglandin E2, leukotriene D2, leukotriene D4

41
Q

What is released from macrophages after they are activated?

A

TNF, IL-1, IL-8

42
Q

What is the result of TNF alpha release?

A

fever, stimulates expression of E-selectin

43
Q

What is the result of IL-1 release?

A

local inflammation, activates endothelium to express adhesion molecules. Induces production of chemokines to recruit leukocytes, system effects: fever, acute phase response, neutrophil production

44
Q

What is the result of IL-8 release?

A

chemotaxis for neutrophils

45
Q

What do NK cells released when activated?

A

IFN gamma

46
Q

What is the result of IFN gamma?

A

activation of phagocytic cells and NK cells

47
Q

What are the three principle tissue changes during acute inflammation?

A

increased blood supply to affected area, increase capillary permeability, increase in leukocyte migration into affected tissue

48
Q

What can often occur during chronic inflammation during infection?

A

granuloma formation to wall off the invader

49
Q

What do sites of acute inflammation have higher numbers of?

A

neutrophils and activated helper T cells

50
Q

What do sites of chronic inflammation have higher numbers of?

A

macrophages, cytotoxic T cells, B cells

51
Q

What cell is the first to present the antigen? What cell is the first to respond to infection?

A

Macrophages phagocytose the invader first, neutrophils are first to respond

52
Q

Describe the response of immune system to invasion?

A

Macrophages phagocytose (1) neutrophils show up, (2) helper T cells, (3) cytotoxic T cells, (4) B cells

53
Q

What is secreted by macrophages to recruit PMNs and CD4+ T cells

A

IL-8

54
Q

What are the three most important cytokines for inflammation?

A

TNF-alpha, IL-1, IFN gamma

55
Q

Describe the steps for leukocyte adhesion

A
  1. Tethering (E-selectin binds to CD15), 2. Triggering (chemokines activate a tethered cell, 3. Adhesion (activation of integrins CR3/LFA-1 from cell with ICAM-1 on epithelium)
56
Q

What two responses can tissue cells do to prevent infection?

A

Send interferons/cytokines to signal IS, make defensins and cathelicidins for antimicrobials

57
Q

What is the signaling of differentiation for Neutrophils?

A

(IL3 + GM-CSF) –> (IL3+GM-CSF + G-CSF)

58
Q

What are the effector cells of acute inflammation or infection?

A

PMNs

59
Q

How do PMNs kill foreign bodies?

A

Fc receptor bind to antibodies; antibody-dependent cellular cytotoxicity

60
Q

What do granules of eosinophils contain?

A

Major basic protein

61
Q

What is major basic protein?

A

potent toxin for helminth worms, induces histamine release from mast cells, activates neutrophils and platelets, can provoke bronchospasm

62
Q

What complement components activate Eosinophils?

A

C5a and C3a

63
Q

What is the signaling for differentiation of eosinophils?

A

(IL3 + GM-CSF) –> (IL3 + GM-CSF + IL-5)

64
Q

What receptors are found of basophils?

A

Fc(epsilon)R1, contains IgE on its cell surface

65
Q

How is histamine released from basophils?

A

IgE on surface is cross-linked by antigen

66
Q

What complement components activate basophils?

A

C5a and C3a

67
Q

What is the signaling for differentiation of basophils?

A

(IL3 + GM-CSF) –> (IL3 + GM-CSF + IL4)

68
Q

What are monocytes called in peripheral tissue, liver, brain and lungs respectively?

A

Macrophages, Kupfer cells, Microglial cells, Bronchial alveolar macrophages

69
Q

What is the signaling for differentiation of monocytes?

A

(IL3 + GM-CSF) –> (IL3 + GM-CSF + M-CSF)

70
Q

What cytokines and lymphokines are produced by macrophages?

A

IFN alpha, IL-1beta, IL-6, TNF alpha, IL-8, IL-12

71
Q

What is the signaling for differentiation of macrophages?

A

IL3 + GM-CSF –> IL3 +GM-CSF + M-CSF –> GM-CSF + M-CSF (REMOVAL OF IL3)

72
Q

Describe classical dendritic cells?

A

process and present foreign protein antigens to T cells

73
Q

Describe follicular dendritic cells

A

passively present foreign antigen in the form of immune complexes to B cells in lymphoid follicles

74
Q

What is the difference between follicular and classical dendritic cells?

A

Classic: present Ag to T-cells; FDCs present to B-cells in lymphoid tissue

75
Q

T/F: NK cells are not from lymphoid progenitors?

A

False; they are from lymphoid progenitors

76
Q

What are important markers of NK cells?

A

CD16 and CD56

77
Q

What do NK cells recognize?

A

damaged cells by a deficiency of MHCI antigen

78
Q

What cytokines activate NK cell killing?

A

Interferons

79
Q

What cytokines activate NK cells to secrete IFN gamma?a

A

IL-12, TNF-alpha

80
Q

What is the signaling for differentiation of NK cells?

A

IL-7 –> IL-2

81
Q

What are severe congenital neutropenias?

A

Lack of ability to produce or maintain a normal level of neutrophils; leads to frequent bacterial infections

82
Q

What is chronic granulomatomas disease?

A

Inability to produce hydrogen peroxide and hypochlorous acid; inability to kill phagocytosed bacteria

83
Q

What is Chediak-Higashi Syndrome?

A

Defect in gene LYST (CHS1), lysosomal trafficking gene that affects lysosomes and melanosomes; problems with pigmentation and also phagocytosis; increased susceptibility to bacterial infections

84
Q

What is Luekcyte adhesion deficiency?

A

Lack of integrin subunit, the common beta chain, inability to recruit innate immune cells to site of inflammation; increased susceptibility to bacterial, fungal and viral infections

IHO Ben (27 decks)

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