The aim of this study was to explore immune activity and molecular mechanism of silkworm peptide. The cell subsets induced by silkworm peptides were detected by flow cytometry. The IFN-γ and IL-4 levels in CD4+ cells were measured by ELISA. TLR2 mRNA expression in mouse CD4+ T cells was detected by qRT-PCR. Western blot was used to detect the protein expression levels of MyD88 and p-IκB. The growth rate of Lewis lung cancer xenografts in mice of the medium-dose group was significantly reduced, and the tumor volume was significantly smaller than that of the control group on the 14th day. The relative vitality values of spleen lymphocytes in the medium-dose and high-dose groups were higher than the control group. The IFN-γ levels in the medium-dose and high-dose groups were significantly higher than the control group. The levels of IL-4 were no significant change among different groups. Compared with the control group, different doses of silkworm peptide groups could increase the levels of NO, IL-6, IL-12, and IL-1β. Compared with the control group, the protein expression levels of MyD88 and p-IκB in 10 μg/ml group and 20 μg/ml groups were significantly increased compared with the control group. Silkworm peptide could induce Th1 activation and M1 type polarization, which was dose-dependent and was relative to the effect of silkworm peptide on inhibiting tumor growth. Silkworm peptide could directly induce M1 type polarization and Th1 activation via TLR2-induced MyD88-dependent pathway in vitro.
Keywords: CD4+ cells; Lewis lung cancer; M1 type polarization; TLR2‐induced MyD88‐dependent pathway; Th1 activation; silkworm peptide.