Type 2 vs Type 3 hypersensitivity

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acciddropping

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Immunology is not my strong subject and hoping someone can make it simpler and help me understand... for the sake of memorizing, I know that serum sickness is type 3 and it can be induced by drugs...and blood transfusion hemolysis is type 2. And for Sulfonamide, it can be type 2 and 3.

But, I want to understand how or why those two are different. Also why is there a "complement mediated cell lysis" with type 2? Hope someone can help. Thanks.

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You're right, this is worth deeply understanding. There's a significant chance you'll be asked to extrapolate this concept outside of must-know diseases.

Type 2 HS = The act of an antibody binding something (the destruction/loss of function of the self-antigen it binds is the pathology)
Type 3 HS = Antibody-antigen bound complex deposition (the immune complexes are floating around in circulation, and the deposition of the complex + associated complement cascade activation and chemotaxis is the pathology)

Complement-mediated cell lysis can occur in T2HS because if the self-antigen happens to be present on cell surfaces, then binding of the antibody can induce MAC formation (remember, the C6-9 complex that forms holes in membranes of pathogens) and kill a cell. It's not the only way T2HS produces pathology, but it's something good to associate with T2HS like you've already done.
 
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Type II: Auto-antibody is targeted to a specific part of the body. Very localized effects.

Type III: Auto-antibody targets something in the blood/serum. Antibody-antigen complexes deposit in random places (although usually in the smaller vessels), and cause highly variable effects.
 
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