Hypersensitivity & Autoimmunity Flashcards

1
Q

Define Hypersensitivity

A

Disorders where normally beenficial parts of an immune response act in an exaggerated or innapropriate fashion to enviromental antigens and cause tissue damage. (bystander damage)

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2
Q

Which types of hypersensitivity are mediated by antibodies?

A

Types I, II & III

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3
Q

What causes type IV hypersensitivity?

A

Innapropriate action of Th1 cells.

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4
Q

What is type 1 hypersensitivity also called?

A

“allergy”

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5
Q

How does Type 1 hypersensitivity arise?

A

enviromental antigens (allergens) are mistaken for pathogens & IgE is innapropriately synthesised.

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6
Q

What does the allergen-specific IgE released during type 1 hypersensitivity do?

A

It trigers mast cells to release inflammatory mediators like histamine & prostoglandins.

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7
Q

What are the consequences of type 1 hypersensitivity?

A
Mucosal Oedema
Capillarly leakage
vasodilation 
ETC
(basically inflammation
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8
Q

What factors influence allergic problems? (think what factors all immune responses arise from)

A
  • Genetic factors
  • Hormonal & neurological influences
  • Enviromental Influences
  • Immune regulatory factors
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9
Q

Why isnt the prescnce of IgE alone enough for an alleric reaction to occur?

A

A clinical allergy arises through many factors not just immune regulatory factors so IgE can be associated with symptoms or not.

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10
Q

What is it called when IgE is present but no smptoms occur?

A

Atopy

A state of sub-clinical immune sensitisation

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11
Q

What antibodies mediate Type 2 hypersensitivity?

A

IgG & IgM antibodies

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12
Q

Why is the line between type 2 hypersensitivy & autoimmune blurreD?

A

Because in type 2 the IgG & IgM antibodies can bind to exogenous or self antigens.

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13
Q

How does type 2 hypersensitivity occur?

A
  • IgG & IgM antibodies target antigens on the surface of cells or within tissues.
  • They cause tissue damage
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14
Q

How do antibodies in type 2 hype cause tissue damage?

A
  • complement activation triggers cell lysis
  • Fc receptors on phagocytes bind to immunoglobulin & phagocytic activity is stimulated
  • antibody dependant cellular cytotoxicity (ADCC)
  • inhibit/stimulate cell function
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15
Q

What is immune complex formation?

A

antigens & antibodies from complexes together.

They are normally transported to the liver/spleen where theyre destroyed by phagoctytes.

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16
Q

How does type 3 hypersensitivity occu?R

A

Predisposing factors in the Ag or the Ab cause the immune complex to precipitate into tissues & cause inflammation

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17
Q

What are the 2 types of inflammation in type 3 hypersensitivty?

A
Serum sickness (immune complexes deposited throughout many tissues)
Arthus reaction (complexes formed locally in tissues)
18
Q

What causes type 4 hypersensitivity?

A

There is an enviromental substance thats strucutrally hard to destroy or an infectious micro-organism that evades the immune system.
The Th1 cells overreact because theyre having trouble destroying the foreign substances.

19
Q

Why do non-infectious enviromental agents need to bind to a host protein to triger type 4 hype?

A

Theyre generally of too low a molecular weight to produce a substantial antigenic stimulus in order to incite an immune resposne.

20
Q

What is a Hapten? (think type 4 hype)

A

The non-infectious enviromental agent bound to the host protein

21
Q

What is a Carrier? (think type 4 Hype)

A

The host protein bound to a low mw enviromental agent.

22
Q

Define an autoimmune disease.

A

Clinical disorders characterised by tissue/organ damage mediated by aberrant cellular and/or humoral immunological mechanisms against autoantigens.

23
Q

Are specific autoantigens organ-specific?

A

They can be localised to certain tissues/organs or spread all over the place.

24
Q

Define tolerance?

A

Process where immune system avoid producing damaging reaction againsts self-antigens.

25
Q

Define central tolerance:

A

Deletion of autoreactive T&B cells during cell maturation

26
Q

Define peripheral tolerance:

A

Inhibiting activity of autoreactive cells that escape central tolerance.

27
Q

In what cases is imune recognition of self not damaging?

A

T cells can recognise antigens complexed to self molecules

Antibodies can recognise/bind to eachtoher to regulate production/activity.

28
Q

What is physiological autoimmunity

A

processes of self-recognition that are normal & beneficial

29
Q

What 5 factors make up the aetiology of autoimmune disorders?

A
  • Genetic factors
  • immune regulatory factors
  • hormonal factors
  • enviromental factors
  • “other”
30
Q

what are immune regulatory factors that help cause autoimmune disorders?

A

defective central or peripheral tolerance mechanisms

31
Q

What “other” factors affect autoimmune disorders?

A

Age
Trauma
Malignant disease

32
Q

What is an early phase response?

A

One that ccurs within minutes

involves preformed mast cell mediators (e.e.g histamine, heparin & chemotactic factors)

33
Q

Whats a late phase response?

A

One that takes hours or days
Involves newly synthesised mediators like prostoglandins
Also Th2 cytokines
Eosinophil mediators

34
Q

What immune effector mechanisms can go wrong to cause an autoimmune disease?

A
  • Cellular (T cell) & antibody (B cell) activity
  • autoantibody acitivation of complement-mediated inflammation
  • immune complex formation (e.g. type 3 hypersensitivity mechanisms)
  • recruitment of innate immune components (phagocytes/cytokines/Nk cells etc)
35
Q

Quick summary of the steps of an autoimmune disorder:

A
  • initiating (enviromental) event [e.g infection] and genetic (susceptibility) factors e.g. inheritence of particular HLA alleles.
  • breakdown of self tolerance
  • autoreactivity (humoral and/or cellular)
  • Tissue damage
36
Q

Do autoimmune disorders only cause damage?

A

No some cause hyperfunction rather than hypo (e.g. hyperthyroidism)

37
Q

How do overlap disorders occur?

A

OFten autoimmune disorders will often occur together if they are both very organ speciic or very not.

38
Q

What factors are involved in the aetiology of autoimmune diseases?

A
  • Immune regulatory
  • Genetic
  • Hormonal
  • Enviromental
39
Q

What are the pathogenic mechanisms of autoimmune disease?

A
  • Immune complex formation
  • Antibody mediated
  • Cell-mediated
  • Recruitment of innate immune components (neutrophils, macrophages etc)
  • complement system
40
Q

List some oran specific diseases:

A
  • Pernicious anaemia (stomach)
  • Adidsons disease (adrenal)
  • Hasimotos thyroiditis, primary myxoedema, thyrotoxicosis (Thyroid)
41
Q

List some non-organ specific diseases:

A
  • Muscles = Dermatomyositis
  • Skin = Scleroderma
  • Kidneys = SLE
  • Joints = Rheumatoid arthritis
42
Q

Name 3 thyroid specific diseases:

A
  • Hashimotos thyroiditis
  • Primary Myxoedema
  • thyrotoxicotis