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SFM Quiz 2 > Innate Imunity > Flashcards

Innate Imunity Flashcards

1
Q

Under host defenses, we have innate and adaptive immunity. What 3 subsets lie under innate immunity?

A

Barriers (skin, cilia, pH, sebum)

Humoral (ROI, Complement, ACPs, Interferons)

Cellular (Neutrophils, basophils, eosinophils, NK, monocytes, macrophage, dendritic, mast)

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2
Q

Under host defenses, we have innate and adaptive immunity. What 2 subsets lie under adaptive?

A

Humoral (antibodies)

Cellular (B cells, helper T cells, cytotoxic T cells)

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3
Q

What includes the barriers in innate

A 
Skin
Mucous epithelia
Ciliated epithelia
Lysozyme
pH
Sebum
Etc.
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4
Q

What’s included in innate humoral immunity

A 
Bactericidal substances
ROI
Complement system
ACPs (acute phase proteins)
Transport proteins
Coagulation proteins
Interferons

Innately, “I, Allergic To Cats, Cant Really Breathe”

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5
Q

What’s included in cellular innate immunity

A 
Blood:
Neutrophils
Eosinophils
Basophils
Monocytes
NK cells

Tissue:
Macrophages
Dendritic cells
Mast cells

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6
Q

What’s included in humoral adaptive immunity

A

Antibodies

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7
Q

What’s included in cellular adaptive immunity

A

B cells
Helper T cells
Cytotoxic T cells

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8
Q

What is sebum made of and how does it inhibit microbe growth?

A

Made up of lactic and fatty acids. Reduces skin pH to 3-5, inhibiting microbe growth

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9
Q

Which specific organs contain IgA (plays a critical role in opsonization of organisms and blocking adherence of pathogens to epithelial surfaces)

A 
Mucous membranes (urinary tract, vagina)
Other (tears, saliva, nasal and bronchial tissues)
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10
Q

What are the 4 cardinal signs of inflammation

A 
Tumor (swelling)
Rubor (redness)
Calor (heat)
Dolor (pain)
*Lasea ( loss of function)
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11
Q

What are the vasoactive mediators involved in inflammation?

A

Prostaglandins and leukotrines
Histamine
Bradykinin

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12
Q

Prostaglandins, Leukotrienes, and Histamine are what kind of cells

A

MAST CELLS

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13
Q

What are the 7 steps of the acute inflammatory response

A
  1. Injury, barrier break, microbe entry
  2. Microbes/injury activates sentinel cells (dendritic, mast, macrophages)
  3. Sentinel cells secrete inflammatory mediators (prostaglandin, leukotrienes, histamine, bradykinin)
  4. There is increased vascular permeability; fluid and proteins enter the tissues
  5. Complement, antibodies, and anti-microbial proteins kill microbes
  6. Adhesion molecules and chemokines cause leukocyte migration into tissue
  7. Phagocytosis and killing of microbes
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14
Q

Why do we get pain w/ inflammation?

A

The inflammatory mediations (bradykinin, prostaglandin, histamine, leukotrienes) stimulate the nerves, causing pain

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15
Q

Is fever caused directly by pathogens?

A

No. Bacterial constituents trigger the production of cytokines TNK, IL-1, IL-6 in macrophages which are potent inducers of the fever response controlled by the hypothalamus.

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16
Q

what kind of receptors are helpful in the innate immune system differentiating between self and non-self

A

PAMPs (pathogen-associated molecular patterns)
*PAMPs are often required for survival of pathogens so that PAMPs cannot be altered, suppressed, or hidden from the pathogen surface

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17
Q

What are the 8 exampled of PAMPs

A
  1. Porins
  2. Lipoproteins
  3. Lipopolysaccharides
  4. Lipoteichoic acid
  5. Teichoic acid
  6. Mannoproteins
  7. Beta-glycan
  8. Lipoarabinomannan

“Manny Beto Teich care of L4 Po”

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18
Q

What is a PRR?

A

Pattern Recognition Receptor

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19
Q

what does the PRR mannose receptor recognize?

A

Mannose PRR recognizes glycan w/ a terminal glycose/ This is important because mannose-tailed glycans are essential surface molecules of bacteria, fungi, and viruses. There are NO mannose-tailed glycans in humans.

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20
Q

which receptors are encoded in the germ-line and therefor have limited diversity?

A

Toll-like Receptor (TLR)
N-formyl methionyl receptor
Mannose receptor

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21
Q

How are receptors distributed? Non-clonal or clonal?

A

Non-clonal. This means that all cells have receptors with identical specificities. This is different than clonal because the B and T cells will have antigen-specific receptors.

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22
Q

How do TLRs work?

A

After recognizing the PAMPs on a microbe, the TLR begins a series of chemical rxns that allows signals to enter the INNATE IMMUNE CELL and allow it to function in the killing of the microbe.

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23
Q

Which TLRs recognize extracellular pathogens?

A

TLR 1,2,4,5,6 ( EXtra is up to SIX…minus the 3!)

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24
Q

Which TLRs recognize intracellular pathogens?

A

TLR 3,7,8,9 (3 skip 3, 7, 8, nINe)

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25
Q

Which signals are produced by NF-KB transcription factor

A

Various cytokines, adhesion molecules, and costimulators. Leading to acute inflammation and stimulation of the adaptive immune system.

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26
Q

What does the transcription factor IRF (interferon regulatory factors) produce?

A

Antiviral cytokines IFN alpha/beta called type 1 interferons leading to the antiviral state

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27
Q

What are the steps of TLR signaling

A
  1. TLR engagement by bacterial or viral molecules
  2. Recruitment of adaptor proteins carried out by Tol-IL-1 Receptor signaling domain
  3. Activation of transcription factors (NF-KB and IRFs)
  4. Increased expression of cytokines, adhesion molecules, costimulators from NF-KB and IFN alpha, beta from IRF)
  5. Acute inflammation, adaptive stimulation, antiviral state
28
Q

What is MyD88

A

myeloid differentiation primary response gene 88. MyD88 is an adaptor protein.

Bacteria use TLR1/2, TLR2/6, TLR4, and TLR5 which stimulate MyD88 which activates the transcription factor NF-KB

29
Q

What is the most important transcription factor (TF) for inflammation?

A

NF-KB (nuclear factor kappa B)

30
Q

Interleukin-1 Receptor Associated Kinase (IRAK) is activated by ____

A

MyD88. MyD88 activates IRAK after the TLR interacts with LPS, viruses, or gram neg bacteria.

31
Q

What 2 actions can be carried out by TRAF, an adaptor protein (TNF receptor-associated Factor 6)

A

It can 1. Inactivate IKB or 2. Induce MAPK kinases.

32
Q

What does the inactivation of IKB or the induction of MAPK kinases lead to?

A

The translocation of NF-KB and the activation of genes in the nucleus.

33
Q

What are some responses of the immunomodulatory genes activated by NF-KB?

A

Influence adaptive response by harnessing T-cells for cell-mediated immunity

Direct antimicrobial response (bacterial death)

Tissue injury (apoptosis of host cells, septic shock)

34
Q

What is the presentation of patients with MyD88 and IRAK-4 deficiency?

A

Susceptibility to infection with either bacteria or viruses.

35
Q

Inflammasomes containing NLRs (nod like receptors) are activated by ____

A

PAMPs activate these cytoplasmic complexes

36
Q

What do NLRs do?

A

They act as scaffolding proteins that assemble signaling platforms that triggers activation of NF-KB and mitogen-activated protein kinase (MAPK) pathways

37
Q

What do inflammasomes activate and what do these things do?

A

THey activate protein caspase-1. Protein caspase-1 processes the inactive cytoplasmic precursor forms into secreted forms of IL-beta and IL-18.

38
Q

What do secreted forms of IL-1beta and IL-18 (produced in the inflammasome) do?

A

They act as potent inflammatory cytokines which drive inflammation

39
Q

What is used to treat gout patients?

A

Anti-IL-1 therapy. IL-1beta is a regulatory key PROinflammatory in gout because it causes the neutrophil influx into the synovial and joint fluid.

40
Q

What are DAMPs

A

DAMPs are endogenous danger molecules released from damaged or dying cells. DAMPs induce non-infectious inflammation by activating the innate immune system by interacting with PRRs (pattern recognition receptors)

41
Q

What are DAMPs recognized by?

A

They are recognized by macrophages via TLRs

42
Q

What are some PRRs

A

TLR
NLR
C-type lectin
etc.

43
Q

Why is necrosis a dirty type of cell death?

A

It is characterized by the swelling and rupture of cell membrane which causes inflammation.

Nucleus: HMGB1, Histones, U1snRNP, DNA/RNA
Mitochondria: ATP, DNA
Cytosol: Urate, S100 Proteins, HSPs, RNA

44
Q

Does apoptosis cause inflammation?

A

No, the apoptotic bodies containing DAMPs are removed by macrophages.

45
Q

What does HMGB-1 signal?

A

Activates NF-KB via TLR3/4 signaling

46
Q

What doe urate signal?

A

Activates NK-KB via NLRP3

47
Q

What do heat shock proteins activate?

A

Activate NF-KB via TLR2/4.

48
Q

What do all DAMPs stimulate the production and release of?

A

TNF-alpha and IL-1

49
Q

How are DAMPs related to autoimmune diseases?

A

DAMPs instigate innate immune pathways that promote adaptive autoimmune responses against self-Ags which manifests as severe clinical sx.
Ex. MS, DMi, Lupus, RA

50
Q

Which ligands are recognized by the TLR1/2 heterodimer

A

Lipopeptides and GPI

51
Q

What are mast cell activators? There are 8

A 
IgE +Ag
PAMPs
Cytokines 
Chemokines 
C3a & C5a complement
Temperature
Pressure
Cell-cell contact
52
Q

What do cytokines mediate?

A

Inflammation, immunity, hematopoiesis

53
Q

Are cytokines a part of humoral or cell-mediated immunity?

A

Humoral. Participate in endocrine, paracrine, and autocrine signaling.

54
Q

What do chemokines help with?

A

Chemokines are small protein chemoattractants important for trafficking immune cells.

Chemokine=chemotaxis

55
Q

Which cytokines are anti-inflammatories

A

IL-10

TGF-beta

56
Q

What is the principal cell source for inflammatory cytokines?

A

Macrophages

57
Q

which cytokine activates NK cells?

A

IL-12. IL-12 acts on NK and T cell, which goes to IFN-gamma to activate macrophages (slide 51)

58
Q

What are the 5 components on the complement system/

A 
MAC
C3b, C3bi
C3a, C4a, C5a
C3b
C4d
59
Q

What does the MAC (complement system) do?

A

Lysis of foreign bacteria and cells

60
Q

What do C3b and C3bi do? (complement system)

A

Opsonization and bacterial phagocytosis

61
Q

What do C3a, C4a, and C5a (complement system) do?

A

Chemotactic anaphylaxtoin and vasodilation (inflammation)

62
Q

What does C3b do? (complement system)

A

Solubilization and clearance of immunocomplexes

63
Q

What does C3d do? (complement system)

A

Enhancement of immune response

64
Q

When neutrophils are coming into the tissue, the endothelial cells must be activated. What are they activated by?

A

Proinflammatory cytokines TNF-alpha and IL-1 produced by active mast cells and tissue-resident macrophages activate endothelial cells, which go on to increase surface expression of P selectin and E selectin adhesion molecules.

65
Q

What is the location of Leukocyte function-associated Antigen 1 (LFA-1) and Very Late Antigen 4 (VLA-4) (how neutrophils come into tissue)

A

They are integrins expressed on neutrophils and monocytes in a low-affinity state

66
Q

What does a chemokine receptor do to LFA-1 and VLA-4 (how neutrophils come into tissue)

A

Chemokine receptors signal to activate LFA-1 and VLA-4 to increase affinity and bind selectively to intracellular adhesion molecule (ICAM-1) and Vascular Cell Adhesion Molecule (VCAM-1) on activated endothelial cells.

SFM Quiz 2 (10 decks)

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