immunology Flashcards

1
Q

function of C3a, C3b, C5a and C5b

A

C3a and C5a - mediators of inflammation and phagocyte recruitment
C3b - opsonization and removal of immune complexes
C5b - formation of MAC, lysis

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2
Q

what is type 2 hypersensitivity

A

IgM and IgG mediated immune response against cell bound or cell associated antigens

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3
Q

what is type 3 hypersensitivty

A

IgM and IgG mediated immune complex deposition (they cant be cleared efficiently and get stuck in things where they cause damage

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4
Q

two outcomes of Type 2 hypersensitivity

A
  • injury due to activation of effector mechanisms (C’, recruitment of inflammatory cells, activation via Fc R)
  • abnormal physiological response by either binding to receptors or proteins interfering with function or by activation/inhibtion
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5
Q

unwanted immune mediated response against foreign ABO blood group antigens is an example of

A

type 2 hypersenstivity responses

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6
Q

why do some people produce antibodies against some drugs

A

because the drug becomes bound to RBCs or platelets which are then the target of anti-drug antibodies

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7
Q

type 2 hypersenstivity involving RBCs leads to

A

haemolytic anaemia or thrombocytopaenia

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8
Q

what is haemolytic disease of the newbord

A

Pregnant mother is Rh positive and foetus is negative. Some RBCs of the foetus will enter the mothers circulation –> mother produces anti-Rh antibodies. With second pregnancy, if foetus if Rh positive –> maternal antibodies will cross the placenta and lyse RBCs of the foetus –> anaemia of the foetus

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9
Q

how do you prevent haemolytic disease of the newborn

A

give mum injection of specific Rh antibody during delivery so that if any foetal RBCs enter maternal circulation, an immune response will be made against them so the mother cant make Ab against Rh

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10
Q

what causes goodpastures syndrome

A

antibodies are made against a variant of collagen type 4 (major component of BM) -> specifically in the kidneys –> complement and phagocyte activation leading to glomerular disease

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11
Q

what are the examples of Type 2 hypersensitivity leading to stimulating and inhibitory Ab

A

stimulatory - graves disease

inhibitory - Myaesthenia gravis

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12
Q

what causes graves disease

A

Abs bind to TSH R on thyroid cells –> stimulates the thymus to produce thyroid hormones –> hyperthyroidism

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13
Q

what causes myaesthenia gravis

A

Ab block the ability of ACh to bind to the R on muscles and therefore no contraction –> atrophy and wasting

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14
Q

when does hype 3 hypersensitivity occur

A

when complexes are excessively produced and inefficiently cleared

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15
Q

how are immune complexes normally cleared

A

by the spleens resident macrophages

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16
Q

what are some reasons that immune complexes can be inefficiently cleared

A

Ag excess
low affinity Ab
inefficient C’ activation

17
Q

how do the immune complexes trigger damage

A

initiate C’ activation –> C3a and C5a inflammatory activation

18
Q

common outcomes of Type 3 hypersensitivity

A

vasculitis
glomerulonephritis
arthritis

19
Q

what causes farmers lung

A

actinomyces in mouldy hay inhaled –> stimulates production of IgG –> alveolitis

20
Q

what is diagnostic of SLE

A

anti-DNA autoantibodies and immune complex deposition in the kidney

21
Q

what are the 2 forms of immunological tolerance

A

central tolerance

peripheral tolerace

22
Q

where and what is central tolerance

A

occurs during development in primary lymphoid organs.

removes self-reactive lymphocytes during development

23
Q

where and what is peripheral tolerance

A

occurs in the periphery

controls self reactive lymphocytes