Thank you for the video, the presentation was great. However i believe you did not explain the pathophysiology well, you mentioned the type 4 H.S reaction as it relates to Psoriasis but never mentioned what could be the specific antigen in this case, you also did not explain why epidermal hyperplasia happens in the first place.
They're not sure about the antigen that triggers psoriasis vulgaris. I've seen LL-37, an antimicrobial peptide produced by keratinocytes, mentioned before as a possible trigger. Then it's the usual: DC to lymf nodes, T-cell activation although I would argue it's both Th1 and Th17, migration to the skin, inflammation. Can't remember which molecule, but probably a T-cell produced interleukin (12, 17, 21 or 22) stimulates keratinocytes to proliferate which causes hyperkeratosis which in turn causes even more LL-37 and cell components which further trigger the immune system
Good job ❤
Thank you so much for this ,well explained !!
Thank you for the video, the presentation was great.
However i believe you did not explain the pathophysiology well, you mentioned the type 4 H.S reaction as it relates to Psoriasis but never mentioned what could be the specific antigen in this case, you also did not explain why epidermal hyperplasia happens in the first place.
They're not sure about the antigen that triggers psoriasis vulgaris. I've seen LL-37, an antimicrobial peptide produced by keratinocytes, mentioned before as a possible trigger. Then it's the usual: DC to lymf nodes, T-cell activation although I would argue it's both Th1 and Th17, migration to the skin, inflammation. Can't remember which molecule, but probably a T-cell produced interleukin (12, 17, 21 or 22) stimulates keratinocytes to proliferate which causes hyperkeratosis which in turn causes even more LL-37 and cell components which further trigger the immune system
@@Bolcjek Thank you so much