What is the immune mechanism involved in type III hypersensitivity reactions?

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Multiple Choice

What is the immune mechanism involved in type III hypersensitivity reactions?

Explanation:
Type III hypersensitivity is driven by immune complex–mediated inflammation. Soluble antigens bind to antibodies in the circulation to form immune complexes. When antibody is in relative excess, these complexes become larger and tend to deposit in tissues rather than being cleared. Once deposited, they activate the complement system, producing fragments that recruit and activate neutrophils. The resulting inflammatory response and enzyme release from neutrophils cause tissue injury at the site of deposition, as seen in conditions like serum sickness and the Arthus reaction. The other options don’t fit because exocytosis is not the mechanism of injury here; type III reactions involve soluble antigen–antibody complexes rather than events focused on secretion, and while any antigen can be involved, the hallmark is immune complex deposition rather than a requirement for heterologous or solely cellular antigens.

Type III hypersensitivity is driven by immune complex–mediated inflammation. Soluble antigens bind to antibodies in the circulation to form immune complexes. When antibody is in relative excess, these complexes become larger and tend to deposit in tissues rather than being cleared. Once deposited, they activate the complement system, producing fragments that recruit and activate neutrophils. The resulting inflammatory response and enzyme release from neutrophils cause tissue injury at the site of deposition, as seen in conditions like serum sickness and the Arthus reaction. The other options don’t fit because exocytosis is not the mechanism of injury here; type III reactions involve soluble antigen–antibody complexes rather than events focused on secretion, and while any antigen can be involved, the hallmark is immune complex deposition rather than a requirement for heterologous or solely cellular antigens.

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