What is the pathogenesis of lichen planus in hepatitis C virus (HCV)?

Updated: Mar 26, 2021
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
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HCV particles are found in immune lymphocytes, macrophages, and dendritic cells, as well as in epithelial cells and cells of blood vessels. [16, 17, 18]

In LP, HCV replicates in OLP epithelial cells of lesional and nonlesional skin cells. What role this plays in developing the LP host response is not known. HCV perturbs the class II host response by impairing the ability of the dendritic or antigen-presenting cell to stimulate a good T-cell response. [19]

Lower expression of interferon gamma and interleukin 12 causes a blunted T-cell response to allostimulatory non–self-related new antigen. Another mechanism of class II immune response inhibition results from the hypervariable region (HVR-1) of envelope protein E2 suppressing CD4+ lymphocytes, which are stimulated to respond to HCV. The HVR-1 acts as a T-cell receptor antagonist. [20]

A theory of causation, termed the superantigen theory of immune stimulation (which includes LP and many other immune-related disorders in which exact causation is a mystery), suggests that the human leukocyte antigen (HLA) class II response was disturbed. Superantigens, such as bacterial proteins and toxins, were proposed to act outside the HLA binding site to broadly stimulate an immune nonspecific response of wide varieties of T cells, including antiself immune responses.

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