Autoimmunity 3 Flashcards

1
Q

How are Type II hypersensitivity complement and Fc mediated inflammation carried out?

A

antibody complexes are deposited in extracellular tissues/matrix

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2
Q

Once antibodies are deposited in tissue, during type III rxn, what are the insuing events?

A

IgG or IgM activate complement which recruits inflammatory cells, causing local tissue damage

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3
Q

Describe the disease mechanism in Goodpasture Syndrome.

A

body produces antibodies agains the basement membrane, particularly apparent in the lung and the kidney

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4
Q

How are Type II hypersensitivity antibody mediated cellular dysfunction inflammation carried out?

A

antibodies are directed against cell surface receptors, which dysregulates cellualr funciton without inflamtion or direct cellular injury (i.e. Graves disease/TSH-R or Myasthenia gravis (Ach-R)

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5
Q

How is type III hypersensitivitity mediated?

A

antigen combines ith anibody in circulation and the resulting immune complex can be deposited in b.v. or tissue, they can also activate complex when deposited

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6
Q

Desposition of immune complex in type II reactions results in what events?

A

antibody complezes activate complex which induces local inflammation; additionally, inflammatory cells may be further activated through Fc-R and platlets may aggregate due to Hagemean factor activaiton (Factor XII)

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7
Q

What is fibrinoid necrosis?

A

acute necorizing vasculitis, immune complex causes lots of inflammation and down stream ischemia

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8
Q

Name 4 diseases caused by immune complex disease and their associated antigen.

A

SLE (DNA/nucleoproteins); Post strep GN (strep cell wall) Polyarteritis Nodosa (hepatitis surface antigen) and reactive arthritis (yersinia bacterial antigen)

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9
Q

How is type IV hypersensitivity mediated?

A

initiated by antigen activated (sensitized) T cells – immune response against intracellular pathogens

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10
Q

What are the two types of cell mediated (Type IV) hypersensitivity.

A

delayed type hypersensitivity (CD4+) and cell mediated cytotoxicity (CD8+)

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11
Q

What cell types cause the inflammation of type IV hypersensitivity.

A

CD4+ cells, both TH1(macrophages) and TH17(neutrophils) cells

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12
Q

How to APC induce macrophage or neutrophil recruitment?

A

APC produce IL-2 (TH1- INF-gamma) to activate macrophages and IL-23 (TH17-IL-17 for neutrophil recruitment

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13
Q

Give an example of a delayed type hypersentivity reaction.

A

tuberculin skin test causes a reaction by CD4+ t-cell if patient was previously exposed to TB

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14
Q

Describe the first exposure that is require dfor a delayed type hypersensitivity.

A

APC present antigen to CD4+ cell and secretes IL-12 causing differentiation of TH1 cells, some of which circulate dna wait for antigen re-exposure

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15
Q

Describe re-exposure in delayed type hypersensitivity.

A

activated TH1 memory cells secrete INF-gamma qhich activates macrophages (the key mediator of DTH)

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16
Q

What is the action of INF-gamma on macrophages?

A

activates macrophages, increases phagocytosis of microbes, increases class II expression for increased antigen presentation and induces secretion of IL-12 for TH1 feedback activation

17
Q

In chronic/presistent antigen delayed type hypersensitivity, how is the immune response modified?

A

granuloma formation occurs, macrophages transform into epithelioid histiocytes and may fuse to form a multinucleated giant cell (which is further surrounded by lymphocytes

18
Q

Describe the mediators/mechanism of cell mediated cytotoxicity.

A

perforins (perforate cell membrane- osmostic lysis) and granzymes (enter perforations and activate caspases) are released on contact with target cell