The observed impairment in TLR-4 signaling in the presence of mHtt was extensive to the synthesis of the mRNAs of anti-inflammatory cytokines IL-10 and TGF-β, leading to the hypothesis that by lowering the synthesis of anti-inflammatory cytokines in MCs in response to innate immune stimulus, mHtt expression could contribute to the systemic pro-inflammatory phenotype observed in HD patients. The gene discussed is TGFB1; the disease is Huntington disease.