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IHO > Innate- Diebs > Flashcards

Innate- Diebs Flashcards

1
Q

What are the 4 main functions of the innate immunity?

A
  1. complement activation
  2. inflammation
  3. Cell activation
  4. Priming of adaptive immune response
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2
Q

What are 2 function of macs?

A
  1. phagocytosis

2. expresses MHC molecules and acts as an APC

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3
Q

Does the innate immunity depend on the recognition by lymphocytes to function?

A

No

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4
Q

What are 3 molecular non self motifs that the innate immunity recognizes?

A
  1. PAMPs
  2. DAMPs
  3. Absences of SELF marker molecules
    - 1 and 2 are phagocytosis
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5
Q

What is the cytoplasmic domain of hetero/homodimerized TLRs? Their function?

A

TIR domain

- recruitment of adaptor proteins

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6
Q

What is the function of TRLs?

A

Recognize PAMPs and signal gene transcription events to combat foreign material. They DO NOT cause phagocytosis

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7
Q

Are neutrophils APCs?

A

NO

- but dendritic cells and macs are

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8
Q

What are the evaginations of phagocytes called around a microbe?

A

Pseudopodia

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9
Q

A defect in NADPH phagosome oxidase cause which disease?

A

Chronic Granulomas disease

  • recurring infections before the age of 5 and after
  • due to a X-linked recessive mostly
  • decrease in bodies reactive species in lysosomes
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10
Q

What are the most common suspects for causing chronic infections in a person with chronic granulomas disease?

A

CATs Need PLACESS to Belch their Hairballs

  • Catalase +
  • Nocardia
  • Pseudomonas
  • Listeria
  • Aspergillus
  • Candida
  • E Coli
  • Staph
  • Serratia
  • B cepacia
  • H pylori
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11
Q

What is the test to confirm chronic granulomas disease?

A

Abnormal dihydrorhodamine (flow cytometry) test. A decrease in green fluorescence

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12
Q

What are some ways that opsonization make microbes more tasty?

A

Coat in CRP,

  • Antibodies
  • Mannose binding lectin
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13
Q

What are opsonins?

A

Phagocytosis enhancing proteins

  • soluble proteins that have bound the the surface of microbes
  • indirect phagocytosis
  • AKA- Soluble pattern recognition proteins
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14
Q

What do opsonins bind to?

A

Many of them bind to repeating components like:

  • carbohydrate structures
  • lipopolysaccharides
  • viral proteins
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15
Q

What are some membrane opsonin receptors on phagocytes?

A

MBL and C1q (like FC region on antibody)

  • structurally similar
  • all bind CD91 opsonin receptor on phagocyte to activate
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16
Q

What is the complement system and its goal?

A

Group of 20 serum proteins which try to control inflammation

- act as a amplifier

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17
Q

What are the 3 ways which complement can act?

A
  1. lysis
  2. Chemotaxis
  3. Opsonization
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18
Q

What is the classical activation of complement?

A

Activated by antibodies or mannose binding lectin

  • C1q bind to Ab/Ag complex
  • cleaves and activated downstream complement response
  • C5b bins to membrane associated with Ab/Ag complex and forms the membrane attack complex
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19
Q

What is the alternative pathway of complement activation?

A

Activated by by microorganisms spontaneously

  • acting as a part of innate response
  • C3 is spontaneously cleaved to C3b Which then binds to bacterial and yeast cells walls as well as virus envelopes
  • Leads to downstream activation of complement components
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20
Q

What physiological changes can happen after complement activation?

A
  • Increased blood flow
  • Increased permeability
  • Release of inflammatory mediators fro mast cells
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21
Q

What are the 3 pathways of which complement can be activated?

A

Classical
Lectin
Alternative

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22
Q

What is the lectin pathway of complement?

A

Mannose Binding lectin bound to bacteria carbs mimics C1q.

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23
Q

What is the function of the a complexes of complement? Ex C3a/C4a/C5a?

A

Act as chemoattractants to increase directional migration of PMNs and macs

  • activate PMN and macs degranulation
  • cause mast cells and basophils to degranulate (histamine)
  • 5>3>4
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24
Q

what is the function of b complexes of complement like C3b or C4b?

A

Deposited on any surface with exposed amine or hydroxyl

  • opsonins
  • cleave more C3
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25
Q

What inactivated complement on our cells?

A

Decay accelerating factor (DAF)

  • AKA CD55
  • Cl esterase inhibitor
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26
Q

what inactivates the Membrane attack complex?

A

CD59- Protectin

Homologous restriction factor (HRF)

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27
Q

What are the hallmarks of Inflammation?

A

Edema
Hyperthermia
Local Hypoxia
Extravasation (WBC’s)

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28
Q

What cytokine recruits neutrophils?

A

IL-8

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29
Q

What are 3 things that trigger inflammation?

A

Complement C5a
Macs
NK cells

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30
Q

What does complement 5a activate?

A

Histamine
Prostaglandin E2
Leukotriene D2
Leukotriene D4

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31
Q

What does prostaglandin E2 cause?

A

vasodilation and increase vascular permeability

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32
Q

What do Leukotrienes D2/4 cause?

A

Neutrophil chemotaxis, increased vascular perm

- increase vascular perm

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33
Q

What doe macs call to action?

A

TNF- fever and E-selectin expression
IL-1- Local inflammation
IL-8- Chemotaxis

34
Q

What do NK cells recruit?

A

INF-y - activation of phagocytic cell and other NK cells

35
Q

What are 3 priniple changes in tissue during acute inflammation?

A
  1. Increased blood supply to affected area
  2. increased cap perm
  3. Increase leukocyte migration in to the affected area
36
Q

What is the principle description of chronic inflammation?

A

Persistent antigenic stimulus and cytotoxic effects of the unresolved infection

37
Q

What the prevalent cells in acute inflammation and chronic?

A

Neutrophils and helper T cells

- Macs, cytotoxic T cells and b cells in chronic inflammation

38
Q

What comes into contact first with a pathogen in the body?

A

Resident phagocytic cells like dendritic cells or macs

- Then neutrophils are the first responders called onto the scene

39
Q

What are the important pro-inflammatory cytokines?

A

TNF-a
IL-1
IFN-y

40
Q

Where is leukocyte migration most likely in the blood stream?

A

Venules - largest and least amount of flow (shear)

41
Q

What is E-selectin and what does it bind?

A

It is an endothelial binding protein that binds CD15 on immune cells.

  • Tethering
  • there is always a small amount of tethering going on at all times.
42
Q

What are the 3 steps of leukocyte adhesion?

A
  1. Tethering- E-selectin
  2. Triggering via chemokines from site of infection
  3. Adhesion via activation of integrins like ICAM-1 (endo) and CR3/LFA-1 on cell
43
Q

What doe tissue cells do for the immune system, whats their purpose?

A

Provide a barrier

  • if infected of damaged signal for help via interferons/chemokines
  • Also produce defensins and cathelicidins to fight against microbes
44
Q

What are the signals (cytokines) for differentiation of polymorphonuclear neutrophils (PMNs)?

A

IL-3 + GM-CSF–> IL-3+ GM-CSF+ G-CSF

45
Q

What are the signals (cytokines) for differentiation of Eosinophils?

A

IL-3 + GM-CSF–> IL-3+GM-CSF+ IL-5

46
Q

What are the signals (cytokines) for differentiation of basophils?

A

IL-3+GM-CSF–> IL-3+GM-CSF+IL-4

47
Q

What are the signals (cytokines) for differentiation of Monocyes

A

IL3+GM-CSF–> IL-3+GM-CSF+M-CSF

48
Q

What are the signals (cytokines) for differentiation of Macs?

A

IL-3+GM-CSF–> IL-3+GM-CSF+M-CSF–> GM-CSF+M-CSF

49
Q

What are the signals (cytokines) for differentiation of dendritic cells?

A

IL-3+GM-CSF–>IL-3+GM-CSF+M-CSF–>GM-CSF+IL-4

50
Q

What are the signals (cytokines) for differentiation of NK cells?

A

IL-7–> IL-2

51
Q

What are some facts about PMNs?

A

Contain granules that dont stain with acidic or basic stains

  • fuse with granule to form phagolysosome
  • Can kill by antibody dependent cellular cytotoxicity
52
Q

What are some facts about eosinophils?

A

Contain Major Basic Protein (MBP)

- activated by C5a and C3a to degranulate

53
Q

What is the purpose of MBP?

A

potent toxin for helminths

  • induces histamine release from mast cells
  • activated neuts and platelets
  • can provoke bronchospasm
54
Q

What are some facts about basophils?

A
  • Activated by C5a and C3a to degran
  • release histamine when IgE cross linked
  • Express FCeR1 for IgE and thus can have IgE on surface
55
Q

What are some differences between basophils and mast cells?

A

Mast cells are not found in circulation

  • Mast cells last weeks/months rather than days
  • MC have proliferative capacity
  • MC mature in the connective tissues
56
Q

What are some cytokines that macs produce?

A

I-NF-a
-IL-1B, IL-6, TNF-a (Fever)
CXCL8 (IL-8) chemotactic factor
- IL-12

57
Q

What is a classical dendritic cell?

A

Eats and presents (APC) to T cells

58
Q

What is a follicular dendritic cell?

A

Passively present foreign Ag in the form of immune complexes to B-cells in lymphoid follicles

59
Q

What are the 3 APC’s and what do they express?

A

DC, Mac, B-cell

  • MHC II thus interact with CD4
  • They also have MHC I because all cells express this
60
Q

What are some facts about NK cells?

A

CD16 and CD56 are important markers

  • recognize damaged cells and deficiency in MHC Ag
  • activated by INF-y
  • IL-12 and TNF-a activated
61
Q

What is severe congenital neutropenia?

A
  • Lack in ability to produce or maintain a normal level of neutrophil
  • leads to frequent bacterial infections
62
Q

What is Chediak-Higashi syndrome?

A

Defect in Gene LYST a lysosomal trafficking gene that affects lysosomes and melanosomes

  • increase susceptibility to bacterial infections
  • autosomal recessive
  • Microtubule dysfunction in phagosome-lysosome fusion
63
Q

What is Leukocyte adhesion deficiency?

A

Lack of LFA-1 integrin (CD18) protein on phagocytes

  • Inability to recruit innate immune cells to site of inflammation
  • increase susceptibility to bacterial, fungal and viral infections
  • autosomal recessive
64
Q

What is significant on the findings of an individual with LAD (leukocyte adhesion deficiency)?

A
  • No pus formation
  • Impaired woud healing
  • Delayed separation of umbilical cord >30 days
  • increased neutrophils but absent at site of infection (why there is no pus formation)
65
Q

What are some significant findings in an individual with suspected Chediak-Higashi syndrome?

A
  • Recurrent pyogenic infections by staph and strep
  • Partially albino
  • peripheral neuropathy
  • progressive neurodegeneration
  • Infiltrative lymphohistiocytosis
  • giant granulocytes and platelets
  • Pancytopenia
  • Mild coagulation defects
66
Q

What is infiltrative lymphohistiocytosis?

A

hyperinflammation caused by uncontrolled proliferation of activated lymphocytes and macrophage

  • proliferation of morphologically benign lymphocytes and macrophages that secrete high amounts of inflammatory cytokines
  • can cause cytokine storm
67
Q

what are some common microbial ligands?

A 
Mannans
B-Glucans
LPS
LTA (Lipoteichoic acid)
Lipopeptides
Diacylglycerides
68
Q

What binds to mannans?

A

Mannose receptor

DC-SIGN

69
Q

What bind to B-glucans of fungi and some bacteria?

A

Dectin 1

70
Q

What binds to LPS and LTA of bacteria?

A

SR-A or scavenger receptors

71
Q

What does SR-B scavenger receptor bind to?

A

LTA, Lipopeptides, B-glucans and diacylglycerides

72
Q

What is the main source of histamine and what is its action?

A

Mast cells and basophils

  • increased vascular perm and smooth muscle contraction
  • chemokinesis
73
Q

What is the main source of serotonin and what is its action?

A

Platelets and mast cells

  • increase vascular perm
  • smooth muscle contraction
74
Q

What is the main source of Platelet activation factor (PAF) and what is its action?

A

Basophils, neuts and macs

  • Mediator release from platelets
  • increase vascular perm
  • smooth muscle contraction
  • neuts activation
75
Q

What is the main source of IL-8 and what is its action?

A

Mast cells, endothelium, monocytes and lymphocytes

- polymorph and monocyte localization

76
Q

What is the main source of C3a and what is its action?

A

Complement C3

- mast cell degran and smooth muscle contraction

77
Q

What is the main source of C5a and what is its action?

A

Complement C5

  • mast cell degran, neuts and macs chemotaxis
  • neuts activation
  • smooth muscle contraction
  • increase capillary perm
78
Q

What is the main source of bradykinin and what is its action?

A

Kinin system (kiniogen)

  • vasodilation
  • smooth muscle contraction
  • increase capillary perm
  • pain
79
Q

What is the main source of prostaglandin E2 and what is its action?

A

Cyclo-oxygenase pathway and mast cells

- vasodilation, potentiates increase vascular perm

80
Q

What is the main source of leukotriene B4 and what is its action?

A

Lipoxygenase pathoway and mast cells

  • neuts chemotoxis
  • synergizes with PGE2 in increasing vascular perm
81
Q

What is the main source of Leukotriene D4 and what is its action?

A

Smooth muscle contraction

increasing vascular perm

82
Q

What is the main source of Fibrono-peptides and fibrin breakdown products and what is its action?

A

Clotting system

  • increase vasuclar perm
  • neuts and macs chemotaxis

IHO (10 decks)

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