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BIOL0027 > Immune Senescence and Inflammation > Flashcards

Immune Senescence and Inflammation Flashcards

1
Q

What is immune senescence?

A

Deterioration of immune system with age - not immune cells in senescent state

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2
Q

Which factors cause different ageing rates in different individuals?

A

Genetic - weak link - importance decreases with age
Environmental - toxin and infectious agent exposure, diet, exercise, microbiota composition - importance increases with age

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3
Q

What is innate immunity and which cell types does it involve?

A

Fast non-specific response

Neutrophils, macrophages, dendritic cells

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4
Q

What is adaptive immunity and which cell types does it involve?

A

Very specific response - long-term memory

T-cells, B-cells

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5
Q

Which aspects of the immune system change with age?

A

Innate immunity
Adaptive immunity
Immune environment (cytokines, hormones)

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6
Q

What are the 2 key features of immune senescence?

A

Loss of antigen-specific immunity and memory

Increased inflammation

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7
Q

Why is a balance between immune action and regulation needed?

A

Immune action protects against cancer and pathogens

Immune regulation needed so no reaction to non-pathogens

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8
Q

How does age affect immune action and regulation and what is the effect of this?

A

Decreased immune action - more prone to infections and cancer
Decreased immune regulation - more prone to autoimmune and inflammatory disease

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9
Q

What does the loss of antigen-specific memory with age involve?

A

Impaired ability to respond to new antigens

Increased frequency and severity of infections from established pathogens

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10
Q

What does the increased inflammation with age involve?

A

Chronic immune cell activation

Increased senescence in non-immune cells - SASP

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11
Q

How does the normal antigen-specific immune response affect pathogen antigen levels?

A

Initial exposure - primary immune response - decreases antigen level
Secondary exposure - faster and stronger immune response - pathogen does not have time to replicate to same level as before - smaller increase in antigen level

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12
Q

How does the aged antigen-specific immune response affect pathogen antigen levels?

A

Initial exposure - primary immune response slow and smaller magnitude - more time for pathogen replication - higher antigen level
Secondary exposure - slower and smaller magnitude response - impaired immune memory

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13
Q

How is the ability to respond to a new antigen (vaccine) changed in older people?

A

Impaired
Smaller increase in T-cells after vaccination - loss of T-cell proliferation (cellular response)
Smaller increase in antibody after vaccination - loss of humoral response

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14
Q

What is the effect of the loss of T-cell memory with age?

A

Loss of control of established virus - reactivation

Increases incidence of established infections

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15
Q

Name a common virus that becomes reactivated in older people

A

VZV (chickenpox/shingles)

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16
Q

What is required for a positive skin test response to VZV?

A

Prior exposure and memory of VZV

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17
Q

What is the difference between the response to the VZV skin test in old and young people and what does this show?

A

Young have positive response - old do not

T-cells do not proliferate in older people - memory lost

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18
Q

How do innate immune cells detect danger?

A

Pathogen-associated molecular patterns (PAMPs) -patterns not found on own cells

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19
Q

How do innate immune cells detect damage of own cells?

A

Host damage-associated molecular patterns (DAMPs)

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20
Q

How do innate immune cells detect PAMPs and DAMPs?

A

Via pattern recognition receptors (PRRs)

21
Q

How do innate immune cells respond to PAMP/DAMP detection?

A

Cytokine secretion
Phagocytosis
Communication to other immune cells

22
Q

How is an antigen-specific response generated?

A

Dendritic cell activation by danger signals - become mature
Picks up antigen - breaks down
Moves into lymph nodes
Costimulatory molecule between dendritic cell and naive T-cell - immunological synapse
Activated T-cells proliferate, secrete cytokines - kill infected cells, help B-cells make antibodies

23
Q

What is the expansion and retraction of adaptive immunity?

A

Expansion - proliferation of specific cells in response to infection
Retraction - once infection resolved most cells die via apoptosis - few remain for memory

24
Q

What are the types of T-cell and the differences between them?

A

Naive T-cells - never detected antigen - slower activation than memory T-cells
Memory T-cells - detected antigen
End-of-life T-cells - may not activate

25
Q

When does T-cell differentiation occur?

A

In response to antigen detection

26
Q

What happens to the innate immune system with age?

A

Impaired phagocytosis, movement, cytokine release, antigen presentation
Preserved numbers

27
Q

What happens to the adaptive immune system with age?

A

Changes at population level - relative proportions of each T-cell type
Intrinsic cellular changes - reduced activation of naive T-cell

28
Q

How does the T-cell population change with age?

A

Numbers stable overall
More end-stage than naive T-cells
More oligoclonal T-cells - from clonal expansion - more cells recognising same antigen - but fewer specificities
Decreased T-cell repertoire
Decreased proliferative response to antigen

29
Q

How does the B-cell population change with age?

A

Decreased number
Decreased antibody production
Decreased antibody affinity
Increased B-cell clonal expansion

30
Q

Where are naive T-cells produced in young people?

A

Thymus

31
Q

Where are naive B-cells produced?

A

Bone marrow

32
Q

What process decreases the number of naive T-cells produced with age?

A

Thymic involution

33
Q

How is the total lymphocyte number kept constant in older people despite thymic involution?

A

Local environment cues promote proliferation of existing cells
Not all cells equally responsive - homeostatic competition favours some clones - over-representation to some specificities - decreases repertoire diversity
Clones not naive
Clones nearer to end-stage - defective

34
Q

How does telomere shortening affect T-cells?

A

Limits number of T-cell divisions

35
Q

The levels of which factors are increased in inflammageing?

A

IL-6
TNF-alpha
CRP

36
Q

What causes inflammageing?

A

Chronic activation of immune cells (macrophages)

Accumulation of senescent immune and non-immune cells (e.g. adipose, fibroblasts)

37
Q

What are the factors contributing to inflammation?

A

Long-term exposure to persistent viruses - keep activating immune system
Obesity - visceral fat inflammatory - accumulates with age
Gut microbiota - in old age gut leakier - microbiota move into blood - activates immune system
Cellular debris and misfolded/misplaced DAMPs - in olde ages cells more likely to malfunction
Senescent cell accumulation - SASP

38
Q

Why do senescent cells accumulate with age?

A

Increased rate of accumulation - due to damage accumulation

Decreased efficacy of senescent cell clearance

39
Q

Which pathways contribute to senescent cell accumulation with age?

A 
Telomere erosion
DNA damage
ROS
SASP from other senescent cells
Activated oncogenes
40
Q

What is the effect of caloric restriction in mice and monkeys?

A

Decreased inflammation
Increased anti-inflammatory molecules
Increased T-cell and innate responses
Increased lifespan

41
Q

How could microbiota composition be manipulated to decrease inflammageing?

A

Diet/prebiotics - to change cell environment

42
Q

What are the effects of a healthy gut microbiota?

A

Decreased systemic inflammation

Increased blood phagocytosis

43
Q

Name 5 potential immune senescence treatments

A 
Thymic regeneration - increase naive T-cell numbers
Cytomegalovirus vaccination
Exercise and stress management
Senescent cell removal
Blocking SASP-related pathways
44
Q

What is a problem with thymic regeneration as a treatment for immune senescence?

A

Ineffective

45
Q

What is the rationale behind the cytomegalovirus vaccination as a treatment for immune senescence?

A

In older people many cells specific for cytomegalovirus - waste of cells - aim to prevent

46
Q

What is the effect of exercise and stress management as a treatment for immune senescence?

A

Exercise decreases systemic inflammation, increases telomerase activity
Chronic stress increases immunosenescence

47
Q

Which of the potential immune senescence treatments are most promising?

A

Senescent cell removal

Blocking SASP-related pathways

48
Q

How can SASP-related pathways be blocked?

A

Metformin

Rapamycin

BIOL0027 (20 decks)

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