ross hypersensitivity type III Flashcards

1
Q

what locations may the immune complexes in type III hypersensitivity deposit?

A

On endothelial cells, in glomerular, in joints (reactive arthritis) and lymphadenopathy.

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2
Q

what factors can affect the function of immune complexes?

A

whether mono or polyvalent Ab
ratio of ab to antigens
affinity and ability to activate complement
ability of host to remove complexes.

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3
Q

What are two examples of type III hypersensitivity reactions?

A

serum sickness and Arthus reaction?

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4
Q

What antigen is targeted by antibodies in the arthus reaction?

A

Often against animal albumin. Occurs when large amount is injected in, where there is an excess of antigen- small complexes and deposition.

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5
Q

What biologic hase been reported to trigger type III hypersensitivity serum sickness against?

A

Against rituximab, high Agn to ab ratio.

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6
Q

How does pathogenesis of Arthus reaction work?

A

local reaction eg. upon vaccines (espeically booter)
Lots of locally administered e.g. peptides, excess ag to ab but in a local area.

Complement activation and mast cell binding and activation.

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7
Q

What autoimmune disease is a good example of type III hypersensitivity? What ab are against?

A

SLE, characterised by anti-nuclear antibodies.

e.g. anti dsDNA, sm/RO, RNP antibodies.

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8
Q

What areas are polymorphisms associated with immune dysregulation in SLE seen?

A

complement, BCR adn TCR signalling, IFN-a (driver for B cell antibody production) and apoptotic aphtways.

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9
Q

Monogenic causes of SLE?

A

C1q, C4, C2 C1r/s. Important for generating C3b/ 3d and C1q importnat for clearnace of apoptotic cells.

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10
Q

What three autoimmune diseases not explained by type III hypersensitivity?

A

antiphospholipid syndrome (seen in SLE patients)
RA
IgG4 associated diseases.

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11
Q

What is target antibodies in anti-phospholipid syndrome and what clinical problems?

A

B2 glycoproteins which are cofactors for phosphlipid proteins.
Causes spordaic thrombi- strokes, deep venous thrombosis, pulmonary embolism.

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12
Q

Why isn’t antiphospholipid syndrome a type III hypersensitivity?

A

Because no immune complexes seen, and Ab seen all the time even when symptoms aren’t present.

(May be triggered by LPS).

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13
Q

Why is RA not a type III hypersensitivity reaction?

A

a lot of people have antibodies against rheumatic factors, by no disease.
Infliximab (anti TNFa is effective in these patients too).
T cells and macrophages are implicated.

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14
Q

What do RA patients die of?

A

cardiovascular disease due to prolonged systemic infection, and even more susceptible to infections ot due to immunosuppression.

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15
Q

What disease is IgG4 associated with?

A

pancreatitis (where there is no cancer)

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16
Q

Why doesn’t IgG4 activate complement?

A

Because it is bispecific and can’t cluster. May just be an artefact of disease.