More importantly, we further demonstrated that the chitin moieties of in vitro-induced sclerotic cells contributed to the inhibition of Dectin-1-mediated Th17 development, although the percentage of Dectin-1+CD11c+ cells in the CD11c-expressing splenocytes, which were considered to include the vast majority of dentritic cells in the murine spleen [33], remained almost unchanged during an i.p. infection with F. pedrosoi. The gene discussed is CLEC7A; the disease is infection.