type ii antibodymediated cytotoxic hypersensitivity1225
TRANSCRIPT
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Type I I
Antibody-mediated
cytotoxic hypersensitivi ty
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The four types of hypersensi tive responses
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Type I I hypersensi tivity reactions (2)
- Innocuous antigens can cause Type II
hypersensitivity reactions insusceptible individuals by bindingto the surfaces of circulating blood cells .
- IgG antibodies against cell-surface receptorsthat disrupt the normal functions of thereceptor, either by causing uncontrollableactivation or by blocking receptor function .
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Antibody-Dependent Cell-mediated Cytotoxici ty (ADCC)
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ABO blood group
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Development of erythroblastosis fetalis (hemolytic disease of the newborn) caused when anRH - mother carr ies an RH + f etus, and effect of treatment wi th anti -Rh antibody, or Rhogam
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Graves’ disease: Hyperthyroidism Myasthenia gravis: Muscle weakness
(hormones) (neurotransmitter)
Effector mechanisms of antibody-mediated disease
C
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Type I I I
I mmune complex-mediated
hypersensitivity
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The four types of hypersensi tive responses
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Type I I I hypersensi tivi ty reactions (1)
- Directed against soluble antigens
- Caused by the deposition of antigen/antibodycomplexes in tissue and blood vessels .
- The complexes activate complement and attract ploymorphs and macrophages to the site.
- These cells may exocytose their granule contentsand release reactive oxygen and nitrogenintermediates to cause local tissue damage .
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Type I I I hypersensi tivi ty reactions (2)
- The deposition of immune complexes intissues causes a local inflammatoryresponse known as an Arthus reaction .
- Serum sickness is a classic example of atransient immune complex-mediated syndrome.
- In situations in which antigen persistssubacute bacterial endocarditischronic viral hepatitissystemic lupus erythematosus (SLE)
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Development of a local ized Ar thus reaction
Immunology (Fig. 16-15), 5th edn 2003 Kuby J
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I mmune complex disease
- The immune complexes produced may bind to vascular endothelium and kidney glomeruli and activate complement(MAC generation).
- It initiates the acute inflammatory responses that destroy the
vessel walls or glomeruli and lead to thrombosis, ischemicdamage to tissues, and scarring.
- Some of the late complement proteins may activate prothrombinases in the circulation that initiate thrombosis .
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Figure 12-23
Serum sickness is a classic example of a tr ansient
immune complex-mediated syndr ome
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Type I V
Delayed-type hypersensitivi ty (DTH )
(Cell-mediated hypersensitivi ty)
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The four types of hypersensi tive responses
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Type I V hypersensi tivity reactions
- T-cell mediated
- 1st group: Tissue damage is caused by the activationof macrophages by TH1 cells , which resultsin an inflammatory response .
- 2nd group: Damage is caused by the activation by TH2cells of inflammatory responses in whicheosinophils predominate.
- 3rd group: Damage is caused directly by cytotoxic Tcells (CTL) .
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Figure 12-24Type I V hypersensi tivity r esponses
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Overview of the DTH response
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Figure 12-26 part 2 of 2The delayed-type (type I V) hypersensitivity r esponse is directed bychemoki nes and cytoki nes released by TH 1 cells stimulated by anti gen (2)
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A prolonged DTH response can l ead to formation of a granuloma
L ytic enzymes released f rom activated macrophages in a
granuloma can cause extensive ti ssue damage.
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A Second Exposure to Poison Oak M ay Result in Delayed-Type H ypersensi tivity
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D l fd l d h i i i f
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Immunology (Fig. 16-20), 5th edn 2003 Kuby J
Development of delayed-type hypersensi tvity reaction aftera second exposure to poi son oak
Secrete INF- γ and other cytokines
Activated macrophages
Secrete mediatorsof inflammation
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Figure 12-28
Blister ing ski n lesions on hand of patient withpoison ivy contact dermati ti s
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There are four types of hypersensi tivity r eaction mediatedby immunological mechanisms that cause ti ssue damage
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