Hypersensitivity 2 Flashcards

1
Q

what is the type 2 hypersensitivity reaction?

A

small molecules that modify cell-surface components perceives as foreign by the immune system

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2
Q

which antibody does type 2 depend on?

what is type 2 also known as?

A

IgG

antibody-dependent cytotoxicity

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3
Q

what are the 3 main aspects of type 2?

A
  1. phagocytes
  2. NK cells
  3. complement mediated cell lysis
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4
Q

describe the process involving phagocytes in type 2

A
  1. epitopes result in normal cell being mistakenly recognised as non-self
  2. IgG bind to epitope
  3. Fc binds to Fc receptor on phagocyte
  4. Lysosome migrates to phagocyte membrane and content is released
  5. Self cell lysis
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5
Q

describe the process involving NK cells in type 2

A
  1. epitopes result in normal cell being mistakenly recognised as non-self
  2. IgG bind to epitope
  3. Fc binds to Fc receptor on NK cell
  4. NK cell releases perforin and granzyme
  5. lysis of self cell
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6
Q

describe the process involving complement activation in type 2

which type of pathway is involved?

A
  1. epitopes result in normal cell being mistakenly recognised as non-self
  2. IgG bind to epitope
  3. C1 binds to bound IgG
  4. MAC form on self cell surface
  5. cell lysis

classical pathway

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7
Q

what can also lead to phagocytosis?

what is ADCC?

A

opsonisation via complement components

antibody dependent cell mediated cytotoxicity

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8
Q

give some examples of type 2 hypersensitivity

A

blood transfusion reactions

haemolytic disease of the newborn (Rh disease)

drug reactions

Myasthenia gravis (ACh receptor)

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9
Q

explain the differences between ABO blood group antigens

A

sugars on the surface of RBCs

H antigen
= N-acetyl glucosamine + galactose + fructose

A antigen
= NAG +Gal + Fuc + N-acetylgalactoseamine

B antigen
= NAG + Gal + Gal + Fuc

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10
Q

why do we have different food groups?

A

having glycosylation of cells in the way microbes get into cells by binding to sugars on the surface

may be less vulnerable to infections by changing sugars on surface

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11
Q

who are the potential donors of each blood group?

why is this?

A

O = O only
(anti A and B antibodies)

A = O or A
(anti B antibodies)

B = O or B
(anti A antibodies)

AB = O, A, B or AB
(no antibodies)

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12
Q

describe hemoltyic disease of the newborn

A

RhD- mother can carry an RhD+ foetus

During delivery placenta can rupture
-> some foetal blood enters mother’s system
-> unrecognised antigen
= immune réponse

foetal RBCs trigger B cells to produce IgG targeting antigen

if there’re subsequent RhD+ children
-> mother will have antibodies that can cross placenta
-> recognise RhD+ RBCs
= lyse cells via type 2 hypersensitivity

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13
Q

describe drug induced reactions

e.g. Penicillin

A

Beta lactam ring of penicillin modified proteins on RBCs

  • > creates foreign epitope
  • > phagocytosis
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14
Q

describe what happens after complement-coated penicillin-modified RBCs are phagocytosed

A
  1. macrophage present peptides from penicillin-protein conjugate
  2. activate CD4 T cells to become Th2 cells
  3. B cells activated bu antigen + Th2 cells
  4. plasma cells secrete penicillin-specific IgG which binds to modified RBCs
  5. activate complement components C1-C9
    -> MAC formation
    = lysis

OR

  1. activates complement components C1-C3
    - > phagocytosis
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15
Q

describe what happens in Myasthenia Gravis

A
  1. motor neurone releases ACh
  2. antibodies recognise ACh receptor
  3. classical complement pathway and immune cell activation
    (4. no muscle contraction)
  4. inflammation
  5. break down muscle membrane
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