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Pathology · Tissue repair: hepatic fibrosis
Sample itemA 45-year-old man with 15 years of chronic hepatitis C has a liver biopsy showing bridging fibrosis. Which cell is the main source of the excess collagen, and what is its principal activating signal?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
C. Hepatic stellate cell activated by TGF-beta and PDGF
Perisinusoidal stellate (Ito) cells normally store vitamin A. After injury, cytokines such as TGF-beta and PDGF from Kupffer cells and damaged hepatocytes turn them into myofibroblast-like cells that lay down type I and III collagen. Persistent activation produces septal fibrosis and eventually cirrhosis.
Option by option
A. Sinusoidal endothelial cell stimulated by VEGF
VEGF acts on endothelium to promote angiogenesis and is not the trigger of matrix production.
B. Hepatocyte undergoing mesenchymal change under HGF
HGF drives hepatocyte proliferation in regeneration and does not turn hepatocytes into collagen producers.
C. Hepatic stellate cell activated by TGF-beta and PDGF (correct)
Activated stellate cells are the principal collagen-producing cells in hepatic fibrosis.
D. Kupffer cell converted to a fibroblast by IL-2
Kupffer cells release the signals but do not transform into collagen-producing fibroblasts under IL-2.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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