Step I Is dermatitis herpetiformis type 2 or 3?

[MudPhud20XX]

Advertisement - Members don't see this ad

So according to FA, the mech of DH is due to the deposits of IgA at tips of dermal papillae. So it does sound like DH is an example of type 2 hypersensitivity, but the FA lecture video just mentioned that DH is an example of type 3 hypersensitivity. If so, how come it's type 3 not 2?

 

[masaraksh]

I think its immune complexes that deposit which makes it type 3. type 2 would be if antibodies were binding to something that is specifically in the dermal papillae (which is not whats happening)


Do you have RObbins, I think I remember reading Robbins for Celiac disease and it was really clear about everything

 

[MudPhud20XX]

So the deposits of IgA is not just IgA alone, right? It's the IgA immune complex that is deposited at tips of dermal papillae, correct?

 

[Burla]

UpToDate says IgA binds transglutaminase, forms an immune complex in the dermis and stimulates neutrophil chemotaxis -> blister

 

[MudPhud20XX]

UpToDate says IgA binds transglutaminase, forms an immune complex in the dermis and stimulates neutrophil chemotaxis -> blister

Makes sense! Since DH is associated with Celiac dz. Thanks!

 

[walakin25]

@MudPhud20XX you sir need to startup another thread like biochem.. that was epic!

 

[Doc-Res]

I remember from Pathoma that deaminated gliadin is presented by APCs via MHC II and Th cells mediate damage. Now, is there a relationship with base excision repair at molecular level? Can anyone help me and clear this ?

 

[Phloston]

IgA immune complexes are the major mechanism, so type 3.

Bullous pemphigoid, pemphigus vulgaris, and SSSS are classic type 2s of the skin.

 

[thehundredthone]

So according to FA, the mech of DH is due to the deposits of IgA at tips of dermal papillae. So it does sound like DH is an example of type 2 hypersensitivity, but the FA lecture video just mentioned that DH is an example of type 3 hypersensitivity. If so, how come it's type 3 not 2?

Because it's a deposit, not so much the actual action of the antibody against antigens on the dermal papillae. Like @Phloston mentioned, those other disease involve a more direct antibody mediated hypersensitivity to various antigens in the skin.

I remember from Pathoma that deaminated gliadin is presented by APCs via MHC II and Th cells mediate damage. Now, is there a relationship with base excision repair at molecular level? Can anyone help me and clear this ?

I'm not sure I understand what you mean. Are you asking if (a problem with) base excision repair causes the gliadin to be deaminated?