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HDM Final > Inflammation, Apoptosis, And Response To Danger Signals > Flashcards

Inflammation, Apoptosis, And Response To Danger Signals Flashcards

1
Q

What type of stimulus might activate the intrinsic apoptotic pathway?

A

Abnormalities in DNA
Lack of O2
Lack of nutrients
Lack of survival signals (mitochondrial dysfunction)

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2
Q

What type of stimuli might activate the extrinsic apoptotic pathway?

A

Removal of survival factors

Proteins of TNF family

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3
Q

The intrinsic pathway is __________-dependent, and occurs in response to injury

A

Mitochondrial

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4
Q

Which apoptotic pathway is mitochondria-independent?

A

Extrinsic pathway

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5
Q

Caspases are first synthesized as an inactive precursor called ________, which must be activated by ________ cleavage at specific sites

A

Procaspases

Protease

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6
Q

Describe the general structure of a caspase after protease cleavage

A

Form a large and small subunit –> form a heterodimer

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7
Q

What are the initiator caspases?

A

Caspase 8

Caspase 9

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8
Q

What is the executioner caspase?

A

Caspase 3

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9
Q

Generation of many molecules of executioner caspases in the caspase cascade result in cleavage of _______ protein and nuclear _______

A

Cytosolic; lamin

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10
Q

The extrinsic pathway of apoptosis involves what two membrane receptor-ligand pairs?

A

FADD:Fas receptor binds Fas Ligand

TRADD:TNF-alpha receptor binds TNF-alpha

[occurs in CD8+ T cells only]

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11
Q

What is the first caspase made by the extrinsic pathway of apoptosis?

A

Caspase 8 (which then combines with caspases 3, 6, and 7)

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12
Q

CD8+ mediated death occurs in part because its expression of ____ increases upon antigenic activation as an anti-inflammatory response

A

FasL

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13
Q

Apoptosis of which cell type carries the risk of bystander damage?

A

CD8+ mediated cell death, due to perforin and granzyme release, even though these are directed at target cell by adhesion molecule binding

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14
Q

What is the difference between inflammation due to microbial attack vs. sterile attack?

A

Microbial attack due to PAMPs

Sterile attack due to DAMPs

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15
Q

Which type of inflammation leads to collateral damage?

A

Chronic inflammation

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16
Q

What are the cardinal signs of acute inflammation?

A 
Pallor/Dolor (pain)
Calor (heat)
Rubor (redness)
Tumor (swelling)
Loss of function
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17
Q

Describe the onset, duration, and specificity of acute vs. chronic inflammation

A

Acute: rapid onset, short duration, non-specific

Chronic: insidious/delayed onset, long duration, specific (involves acquired immunity)

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18
Q

What are the cardinal signs of chronic inflammation?

A

Cardinal signs are absent in chronic inflammation

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19
Q

What are the causative agents of acute inflammation?

A

Physical and chemical damage

Pathogen invasion

Tissue necrosis

Immune response

20
Q

What are the causative agents of chronic inflammation?

A

Persistent infection

Presence of foreign bodies

Autoimmunity

21
Q

What are the fundamental cells involved in acute inflammation?

A

Neutrophils

Mast cells

Platelets

Basophils

[in addition to all their soluble mediators]

22
Q

What are the fundamental cells involved with chronic inflammation?

A

B and T lymphocytes
Macrophages
Plasma cells
Antibodies

23
Q

Inflammation is resolved by ___________, which clean up cellular debris utilizing a special type of PRR called _________ receptors.

Specialized anti-inflammatory cytokines include IL-10 and TGF-beta

A

M2 macrophages

Scavenger

24
Q

How does necrosis compare to apoptosis in terms of cellular size and # of cells affected?

A

Necrosis: cell swelling, many cells affected

Apoptosis: cell shrinkage, one cell affected

25
Q

How does necrosis compare to apoptosis in terms of cellular content uptake and inflammation?

A

Necrosis: cell contents ingested by macrophages, significant inflammation

Apoptosis: cell contents ingested by neighboring cells, no inflammation

26
Q

How does necrosis compare to apoptosis in terms of membrane integrity?

A

Necrosis: loss of membrane integrity, cell lysis occurs

Apoptosis: membrane blebbing, but integrity maintained, apoptotic bodies form

27
Q

How does necrosis compare to apoptosis in terms of organelles?

A

Necrosis: organelle swelling and lysosomal leakage, random degradation of DNA

Apoptosis: mitochondrial release of pro-apoptotic proteins, chromatin condensation and non-random DNA degradation

28
Q

_________ are molecules released by stressed cells undergoing nerosis that act as endogenous danger signals to promote and exacerbate the inflammatory response

A

DAMPs

29
Q

DAMPs are also called _______

A

Alarmins

30
Q

Binding of DAMP ligands to _____ induces intracellular signaling in the phagocytes leading to their activation

A

PRRs

31
Q

What are some examples of DAMPs due to cell necrosis?

A 
dsRNA
CpG
Uric acid
HMGB1
ATP
HSP
IL-1alpha
32
Q

What are some DAMPs associated with ECM degradation?

A

Hyaluronan

Heparan sulphate

33
Q

______ is a significant alarmin responsible for activating a cell by binding its receptor HMGB1 (high mobility box 1)

A

RAGE

34
Q

True or false: DAMPs are non-infectious, associated with cell damage or necrosis, and may occur due to radiation, surgery, burns, UV light, etc.

A

True

35
Q

The signaling system for detection of pathogens and stressors involves the assembly of a ________ sensor and adaptor, and the inactive caspase into the ________________ - which activates the caspase which in turn results in expression of IL-1

A

NLRP-3

Inflammasome

36
Q

The inflammosome results in the production of what 2 potent inflammatory cytokines?

A

IL-1

IL-18

37
Q

What is SIRS?

A

Systemic inflammatory response syndrome = pathogenic overstimulation of the immune response

38
Q

What is the effect of non-infectious SIRS?

A

Caused by DAMPs, leads to shock

39
Q

What is the effect of infectious SIRS?

A

Sepsis –> septic shock

40
Q

What are the symptoms associated with systemic SIRS and sepsis?

A

Fever
Tachycardia
Tachypnea
Leukocytosis

41
Q

What symptom is characteristic of severe SIRS or severe sepsis?

A

Organ failure (due to lack of perfusion)

42
Q

What symptom is characteristic of shock or septic shock?

A

Hypotension

43
Q

What is the typical cytokine profile of SIRS?

A

IL-1
IL-6
TNF-alpha

[these are the acute phase cytokines, which stimulate the liver to make more APPs including CRP and C’ –> cytokine storm]

44
Q

Symptoms of SIRS appear during the hyper-inflammatory phase. The patient’s immune system will try to provide a ______

During this period, the patient is significantly _________

The immune system will rebound again with a hyperinflammatory reaction, leading to another compensatory response. Each one becomes less severe until _______ is reached

A

CARS (compensatory anti-inflammatory response)

Immunosuppressed

Homeostasis

45
Q

______ is an inherited disorder of abnormal lymphocyte survival caused by dysregulation of the Fas apoptotic pathway

A

ALPS (autoimmune lymphoproliferative syndrome)

46
Q

ALPs leads to an excess of what cell types?

A

TCR alpha/beta CD3+CD4-CD8- (double negative T cells)

These will accumulate in the LNs, spleen, and peripheral blood - results in lymphoproliferation, autoimmune disease, and malignancy

HDM Final (12 decks)

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