Our group has provided evidence suggesting that surface expression of TLR2 on both B cells and DCs is significantly higher in helminth-infected MS patients (Figure 2) and that exposure of either cell population to soluble egg antigen (SEA) obtained from S. mansoni resulted in significant upregulation of TLR2 in helminth-infected MS patients, but not in uninfected individuals (Figure 3; Correale and Farez, 2009). The gene discussed is TLR2; the disease is myeloid sarcoma.