Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BM 212: Introduction to Immunology > Block E Lecture 3: Chronic Inflammation and Autoimmunity > Flashcards

Block E Lecture 3: Chronic Inflammation and Autoimmunity Flashcards

1
Q

What happens if the inflammatory response persists even after clearing the antigen?

A

Chronic inflammation and systemic effects
(Slide 3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is chronic inflammation?

A

A pathological condition (disease or disorder) involving persistent, increased expression of inflammatory cytokines
(Slide 4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is an example of chronic inflammation?

A

Type II diabetes
(Slide 4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What 4 conditions does Type II diabetes exacerbate (make worse)?

A

Heart disease
Alzheimer’s
Autoimmunity
Cancer
(Slide 4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What 2 categories can causes of chronic inflammation be divided into?

A

Infectious and non-infectious causes
(Slide 4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is an infectious cause of chronic inflammation?

A

Chronic infections - pathogens not being cleared hiding or evading the immune system, continuously triggering inflammation
(Slide 5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is an example of a non-infectious cause of chronic inflmmation?

A

Obesity - visceral fat cells can be stimulated to produce inflammatory cytokines
(Slide 5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What 4 factors do the consequences of chronic inflammation vary depending on?

A

Tissue of origin
Sex
Age
Health status
(Slide 6)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What 3 cytokines show increased levels in chronic inflammation?

A

IL-1, IL-6and TNF-α
(Slide 6)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can inflammatory cytokines IL-1, IL-6 and TNF-α contribute to?

A

Insulin resistance (Causing Type II diabetes)
(Slide 6)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What 4 things can inflammatory cytokines IL-1, IL-4 and TNF-α induce in chronic inflammation?

A

Scar tissue
Organ dysfunction
Cell proliferation
Angiogenesis (the formation of new blood cells)
(Slide 6)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is self-tolerance?

A

The process of defining ourselves from foreign cells / antigens / allergens
(Slide 8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What antigens other than self are tolerated by the body?

A

Benign and beneficial ones
(Slide 8)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does the immune system do on top of ignoring self-antigens?

A

Recognises and protects self-components and beneficial commensals (microbes)
(Slide 9)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What were T-regulatory cells (Tregs) formally known as?

A

Suppressor T-cells - useful to know for old papers
(Slide 9)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where does central tolerance occur?

A

Primary lymphoid organs - Thymus for T-cells, bone marrow for B-cells
(Slide 10)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where are Tregs formed?

A

The thymus
(Slide 11)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Do surviving T cells from central tolerance recognise self-antigens?

A

No
(Slide 11)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Do surviving regulatory T cells (Tregs) from central tolerance recognise self-antigens?

A

Yes
(Slide 11)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is positive selection of T cells?

A

T-cells undergo selection in the thymus to ensure they can recognise and respond to antigens presented by MHC receptors. T cells that cannot interact with self-MHC molecules undergo apoptosis and those that interact successfully receive signals for survival
(Slide 11)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is negative selection of T cells?

A

The elimination or inactivation of T cells that strongly recognise MHC receptors, preventing autoimmunity from self-reactive T cells
(Slide 12)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is clonal selection?

A

The activation and differentiation of effector lymphocytes that recognise the foreign antigen
(Slide 12)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What 3 expression are Tregs identified by?

A

FOXP3, CTLA-4 and CD25
(Slide 13)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do Tregs do?

A

Suppress or “regulate” autoimmune responses to self-antigens in the periphery
(Slide 13)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Are the majority of Tregs CD8+ or CD4+?

A

CD4+
(Slide 13)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is one way used by Treg cells to inhibit APCs?

A

Their CTLA-4 physically interacts with CD80/CD86 (B7-1/B7-2), preventing the interaction between these co-stimulatory molecules and CD28 on conventional T cells. This inhibits the activation of effector T cells
(Slide 14)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How can activation of indoleamine 2,3-dioxygenase (IDO) by Treg cells create an immune-inhibitory environment?

A

As they convert tryptophan to kynurenine
(Slide 14)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does IL-2 do?

A

It stimulates proliferation and growth of helper and cytotoxic T cells
(Slide 14)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do Tregs absorb local IL-2?

A

Via CD25
(Slide 14)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What kind of cytokines do Tregs make?

A

Inhibitory cytokines
(Slide 14)

31
Q

What 3 ways can auto-immune diseases be mediated?

A

Anti-body mediated, Cell-mediated or a mix of both
(Slide 16)

32
Q

What causes auto-immune diseases?

A

The destruction of self-proteins, cell and organs
(Slide 16)

33
Q

What are the 2 categories of auto-immune disease?

A

Organ-specific or systemic
(Slide 16)

34
Q

How do genetics play a role in autoimmunity?

A

Particular class I and II MHC alleles or mutations are associated with auto-immune diseases
(Slide 17)

35
Q

What do people with MHC class I and II alleles and mutations associated with particular immune events still need on top of this to develop the auto-immunedisease?

A

A trigger event from the environment
(Slide 17)

36
Q

Is auto-immunity more prevalent in males or females?

A

Females
(Slide 17)

37
Q

Name 3 examples of auto-immune diseases with genetic associations.

A

Type 1 Diabetes
Rheumatoid arthritis
Multiple Sclerosis
Crohn’s disease
Systemic lupus erythematous
(Slide 17)

38
Q

What are 3 factors that may account for females being more susceptible to auto-immune diseases than males?

A

Hormonal differences
Conception and pregnancy
Gut microflora after puberty
(Slide 18)

39
Q

What 5 factors are believed to cause autoimmunity?

A

Diet
Obesity
Smoking
Infection
Mucosal flora
(Slide 19)

40
Q

How can infection result in auto-immunity developing?

A

Tissue pathology following infection may result in the release of sequestered (hidden) antigens the immune system hasn’t encountered before, which can be presented by APCs in a way that promotes immune activation.
The molecular components of certain microbial antigens may share strong similarities to self-antigens resulting in cross-reactive responses
(Slide 20)

41
Q

Is Hashimoto thyroiditis organ specific or systemic ?

A

Organ-specific
(Slide 22)

42
Q

What is Hashimoto thyroiditis?

A

Production of auto-antibodies and sensitised Th1 cells specific for thyroid antigens thyroglobulin and thyroid peroxidase - with binding to this proteins interfering with iodine uptake
(Slide 22)

43
Q

What does Hashimoto thyroiditis result in?

A

Hypothyroidism (underactive thyroid)
(Slide 22)

44
Q

What are 3 symptoms of Hashimoto thyroiditis?

A

Fatigue
Lethargy (lack of energy)
Unexplained weight gain
(Slide 23)

45
Q

What does therapy for Hashimoto thyroiditis involve?

A

Daily administration of the lost thyroid hormone thyroxine
(Slide 23)

46
Q

What is Myasthenia?

A

Production of auto-antibodies against the acetylcholine receptors (AChRs) on the motor end plates of muscles, blocking the normal binding of acetylcholine and inducing complement-mediated lysis of the cells
(Slide 24)

47
Q

What are the 2 symptoms of the progressive weakening of the skeletal muscles due to Myasthenia?

A

Drooping eyelids
Inability to retract the corners of the mouth
(Slide 25)

48
Q

What 3 things does the treatment of Myasthenia involve?

A

Increasing acetylcholine levels
Decreasing antibody production via immuno-suppressants
Removing antibodies via the removal and exchange of blood plasma
(Slide 25)

49
Q

What occurs in systemic auto-immune diseases?

A

Auto-reactive cells recognise a target antigen or antigens found in multiple tissues or organs resulting in inflammation and physiological disruptions at multiple locations within the body
(Slide 26)

50
Q

What tissue damage occurs in systemic autoimmune diseases?

A

Wide-spread tissue damage
(Slide 26)

51
Q

What 4 things can the wide-spread tissue damage as a result of systemic auto-immune diseases driven (Controlled) by?

A

Cell-mediated immune activity, auto-antibodies, accumulation of immune complexes or a combination of these
(Slide 26)

52
Q

What is the typical age range where systemic lupus erythematous onsets?

A

20 - 40 years old
(Slide 27)

53
Q

Does systemic lupus erythematous have a genetic link?

A

Yes
(Slide 27)

54
Q

What 2 cells are auto-antibodies generated against in systemic lupus erythematous and what can this lead to?

A

Red blood cells and platelets leading to complement-mediated lysis of the cells
(Slide 28)

55
Q

What does systemic lupus erythematous cause?

A

Haemolytic anaemia and then thrombocytopenia
(Slide 28)

56
Q

What is haemolytic anaemia?

A

A disorder in which red blood cells are produced faster than they can be made
(Slide 28)

57
Q

What is thrombocytopenia?

A

Deficiency of platelets in the blood
(Slide 28)

58
Q

What do immune complexes do in systemic lupus erythematous do and what type of hypersensitivity is it?

A

Type III hypersensitivity - immune complexes of auto-antibodies and nuclear antigens are deposited along the walls of small blood vessels
(Slide 28)

59
Q

What do immune complexes deposited alone walls of small blood vessels activate in systemic lupus erythematous?

A

The complement cascade and generation of membrane attack complexes (MAC)
(Slide 28)

60
Q

What can occur in severe cases of systemic lupus erythematous?

A

Excessive complement activation produces elevated serum levels of complement fragments - leading to neutrophil aggregation and attachment to vascular endothelium
(Slide 28)

61
Q

What are 5 signs / symptoms of systemic lupus erythematous?

A

Fever
Weakness
Arthritis
Kidney disfunction
Skin rashes
(Slide 29)

62
Q

Does rheumatoid arthritis have a genetic susceptibility element?

A

Yes
(Slide 31)

63
Q

What is the typical age range in which rheumatoid arthritis onset occurs?

A

Between 40 and 60 years old
(Slide 31)

64
Q

Is rheumatoid arthritis an antibody or cell-mediated disease?

A

It’s both
(Slide 31)

65
Q

What 2 things do auto-antibodies target in rheumatoid arthritis?

A

Citrullinated proteins and rheumatoid factor (RF)
(Slide 31)

66
Q

What type of hypersensitivity reaction is rheumatoid arthritis?

A

Type III
(Slide 33)

67
Q

What 5 immune cells are involved in rheumatoid arthritis?

A

Macrophages
Dendritic cells
Neutrophils
Natural Killer cells
T-cells
(Slide 34)

68
Q

What 3 pro-inflammatory cytokines do CD4+ T helper 1 (Th1) cells induce and what does this lead to in rheumatoid arthritis?

A

IFN-gamma, TNF-α, IL-2 leading to cartilage destruction and bone erosion
(Slide 35)

69
Q

What are Th17 cells?

A

A large subset of CD4+ Th cells which can provide large numbers of cytokines such as IL-17A and IL-17F
(Slide 35)

70
Q

What diseases are Th17 cells thought to play an important role in developing?

A

Immune-mediated diseases
(Slide 36)

71
Q

How does Th17 play a part in the development of rheumatoid arthritis?

A

IL-17 they secrete triggers changes in the synovium that lead to synovitis and maintain inflammation in the joint
(Slide 36)

72
Q

What are 4 symptoms of rheumatoid arthritis?

A

Answers include:
Pain or arching in more than 1 joint
Stiffness in more than 1 joint
Tenderness and swelling in more than 1 joint
The same symptoms in both sides of the body (i.e in both hands or both knees)
Weight Loss
Fever
Fatigue or tiredness
Weakness
(Slide 37)

73
Q

What are 4 immunotherapies for systemic auto-immune diseases?

A

General immune suppression - with immuno-suppressants
Immunosuppression of specific cells/pathways
Drugs to block co-stimulation
Re-establishing tolerance
(Slide 38)

BM 212: Introduction to Immunology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions