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I'm only asking this to confirm simply bc FA, on pp. 233-4 and 420, doesn't mention it.
Is Reiter syndrome merely a type-II hypersensitivity reaction based on cross-reactivity? Or is there an additional mechanism in place?
Given that most patients are HLA-B27 positive and HLA-A, B, C all encode MHC-I receptors, I'd assume the damage is mainly CD8+-mediated, which would eliminate type-IV hypersensitivity as a mechanism and further support type-II.
Yet again, immuno isn't my strong point, so any thoughts?
Cheers,
Is Reiter syndrome merely a type-II hypersensitivity reaction based on cross-reactivity? Or is there an additional mechanism in place?
Given that most patients are HLA-B27 positive and HLA-A, B, C all encode MHC-I receptors, I'd assume the damage is mainly CD8+-mediated, which would eliminate type-IV hypersensitivity as a mechanism and further support type-II.
Yet again, immuno isn't my strong point, so any thoughts?
Cheers,
