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WEEK 12 SEM 4 > Disorders of the Immune System > Flashcards

Disorders of the Immune System Flashcards

1
Q

What is hypersensitivity?

A

exaggerated or innapropriate immune response

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2
Q

What does hypersensitivity result in?

A

tissue damage

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3
Q

What is hypersensitivity classified into?

A

type I
type II
type III
type IV

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4
Q

What is type I hypersensitivity?

A

allergic response provoked by re-exposure to antigen

there are 2 stages

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5
Q

What are the 2 phases of hypersensitivity I?

A
  1. sensitization phase

2. effector phase

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6
Q

What happens in the sensitization phase of type I hypersensitivity (use pollen as allergen)?

A
  1. first exposure to pollen
  2. B lymphocytes recognise antigens
  3. B lymphocytes bind to antigen and internalize them
  4. B cells present antigen to Th2 cells
  5. Th2 secretes IL4
  6. causes B cells to switch class and become IgE producing cells
  7. IgE circulates
  8. IgE comes into contact with mast cells
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7
Q

On what region of mast cells do the antibodies bind?

A

antibodies have Fc region
Mast cells have Fc receptors
antibodies bind to this region
now mast cells can recognise the antigen

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8
Q

What happens in the effector phase of type I hypersensitivity?

A
  1. 2nd exposure to pollen
  2. mast cells recognise antigen and bind to it
  3. single pollen binds to 2 IgE antibodies
  4. lead to immediate phase reaction
  5. this will lead to an latent phase reaction
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9
Q

What is immediate phase reaction?

A

release of vasodilator amines such as histaminefrom the mast cell

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10
Q

What is type II hypersensitivity?

A

when antibodies bind to host cell antigens on cell surface

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11
Q

What are examples of type II hypersensitivity?

A

myasthenia gravis
rhesus isoimmunization
grav’es disease

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12
Q

What is myasthenia gravis?

A

antibodies produced against nicotinic Ach receptors
receptor gets blocked
no muscle contraction

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13
Q

What is rhesus isoimmunization?

A

RhD is antigen carried by RBC

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14
Q

If a father is RhD positive and a mother is RhD negative and mother gets pregnant with an RhD positive baby, what does the mother produce?

A

anti-RhD antibodies (IgM)

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15
Q

Why can’t IgM cross the placenta?

A

IgM is too big

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16
Q

If a mother gets pregnant again and the first child was RhD positive, what happens in the second pregnancy?

A

memory B cells stimulated

anti RhD antibodies (IgG) can cross the placenta and lyse the foetal blood

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17
Q

What type of disease is Grave’s Disease?

A

autoimmune- high levels of thyroid hormone are produced

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18
Q

What does the body produce in Grave’s disease?

A

autoantibodies to TSH receptor

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19
Q

What do autoantibodies in Grave’s Disease do?

A

bind to and stimulate the TSH receptor on the thyroid gland
more thyroid hormone release
hypertrophy of thethyroid gland

20
Q

What do high levels of thyroid hormone do?

A

turn down TRH and TSH

21
Q

What is type III hypersensitivity?

A

when antibodies target soluble circulating antigens

22
Q

In Lupus, against what are the autoantibodies made?

A

self molecules such as DNA and nuclear ribonucleoproteins

23
Q

How do autoantibodies work in Lupus?

A

bind to self molecules

form immune complexes

24
Q

What can immune complexes in Lupus do?

A

recruit complements to attack self cells

get deposited in glomerulus of the kidney- lead to glomerulonephritis

25
Q

What things are seen in Lupus patients?

A
  • abnormal B cell activation
  • B cells become more sensitive to stimulatory cytokines
  • B cells can polyclonally activate
  • changes in cytokine levels
  • T cell function changes
  • phagocytic cells do not function properly,
26
Q

What happens in Type IV hypersensitivity?

A

T cell mediated

27
Q

What test is used to screen for Tb?

A

Mantoux

28
Q

What are examples of Type IV hypersensitivity?

A 
Mantoux test for Tb
Type I diabetes
Coeliac disease
Ulcerative colitis and Crohn’s disease
Psoriasis
29
Q

What happens in the mantoux test?

A
  1. inject patient with mycobacterial antigen extract under the skin
  2. macrophages engulf antigen
  3. present antigen coupled with MHC II to CD4+ cells
  4. specific Th cells will get activated and then release cytokines that activate the macrophage and cause it to release cytokines
  5. get firm red swelling of skin
30
Q

How is type I diabetes a Type IV hypersensitivity reaction?

A
  1. beta cells in the islets of Langerhans of the pancreas act as the autoantigen
  2. APC engulf these and present the peptides complexed with MHC II
  3. stimulates corresponding CD4+ T cells that release cytokines to activate cytotoxic T lymphocyte
  4. they damage the beta cells and insulin cannot be produced
31
Q

How is coeliac disease a Type IV hypersensitivity reaction?

A
  • genetically predisposed
  • HLA gene is somehow important (it codes for MHC proteins)
  • patients have IgA anti-gliadin, anti-endomysium and anti-reticulin antibodies
  • gliadin is a component of gluten and reticulin and endomysial proteins are host proteins
  • these antibodies are believed to be released from the intestine where T-cells are also present
  • there is inflammation, resulting in damage to intestinal mucosa so we see villous atrophy and malabsorption
32
Q

What is coeliac disease?

A

When person is intolerant to gluten

33
Q

What happens in Ulcerative colitis and Crohn’s disease

A
  • changes in the proportion of T and B cells
  • it is seen that there are a large number of B cells producing autoantibodies to the intestinal mucosa
  • there is also complement deposition in the intestinal mucosa
  • this could have possibly occurred due to presentation of autoantigens on MHC II by antigen presenting cells to CD4+ T helper cells-this naturally results in increased interleukin levels
34
Q

What is seen in high numbers in psoriasis?

A

CD4+ cells seen in skin

35
Q

What is good treatment for psoriasis?

A

immunosuppressive treatments such as UV therapy are effective. suggesting that these cells are involved

36
Q

What is autoimmunity?

A

acquired immune reaction to self antigens

37
Q

What are causes of autoimmunity?

A 
age
gender
infection
genetics- HLA
specific autoantigens
drugs
immunodeficiency
38
Q

What is primary immunodeficiency?

A

this happens due to problems with complements, phagocytes, humoral immunity or cellular immunity

39
Q

What are examples of primary immunodeficiency (problems with complement)?

A

C1q inhibitor deficiency

C3 deficiency

40
Q

What is C1q inhibitor deficiency?

A

this results in hereditary angioedema due to continuous complement activation

41
Q

What happens in C3 deficiency?

A

complement cascade cant occur without C3

so you get recurrent infections

42
Q

What are problems with phagocytes (in primary immunodeficiency)?

A

chediak higashi syndrome

43
Q

What happens in chediak higashi syndrome?

A

phagocytes cant form phagolysosomes

so phagocytosed bacteria cant be destroyed

44
Q

What are problems with B cells (in primary immunodeficiency)?

A

severe combined immunodeficiency syndrome
hyper IgM syndrome
common variable immunodeficiency

45
Q

What are problems with T cells (in primary immunodeficiency)?

A

lack of thymus or hypoplastic thymus-this is seen in DiGeorge syndrome (22q11 deletion)

46
Q

What happens in secondary immunodeficiency?

A

this is due to a result of external forces
e.g.
HIV-CD4+ count drops leading to AIDS
-malnutrition
-tumors-some cancer cells can release immunosuppressive factorsthis is treated using cytotoxic drugs and radiation

WEEK 12 SEM 4 (5 decks)

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