Hyperacute = minutes to hours, host preformed Ab against graft endothelial cell Ag = compliment activation, endothelial damage, inflammation (within the tissue, NOT interstitium), clotting cascade, ischemic necrosis and thrombosis. https://tpis.upmc.com/tpislibrary/kidney/KHAcuRej.html

Acute = weeks to months = graft Ag activates host CD4 and CD8 T cells leading to parenchymal cell damage, interstitial lymphocytic infiltration, and endotheliaitis. https://tpis.upmc.com/tpislibrary/kidney/KARejMod.html

Chronic = months to years, chronic DTH (type IV hypersensitivity) reaction in vessel wall leading to intimal smooth muscle cell proliferation and vessle occlusion, with biopsy showing narrowed vascular lumen and extensive smooth muscle.

GVHD = graft cells (most typically bone marrow transplants) recognize host cells as self/foreign and lead to destruction of host tissue leading to rash, jaundice, diarrhea, and GI hemorrhage (this occurs because most bone marrow transplant patients have undergone full radiation which attacks the rapidly providing cells most (i.e. skin, GI mucosa, hair, hepatocytes) so graft destruction of host cells in those areas leads to symptoms).

https://tpis.upmc.com/

This is a case of acute transplant rejection. weeks to months after the transplant, recipient cd8 and/or cd4 t cells are activated against the donor (a type 4 HSR) and the donor starts making antibodies against the transplant. This presents as a vasculitis with dense interstitial lymphocytic infiltrates. (FA2018 pg 119)

page 119 FA Patient is presenting months after the transplant, which means it can't be hyperacute unless he stopped taking his immunosuppressants. Acute/chronic/GVH disease are mediated by T cells for the most part (I think), so this would mean lymphocytic infiltrates.

Can anyone explain why Fibrous scars with plasma cells is not the correct answer?