| First Author | Liu H | Year | 2017 |
| Journal | Oncoimmunology | Volume | 6 |
| Issue | 4 | Pages | e1292195 |
| PubMed ID | 28507796 | Mgi Jnum | J:256594 |
| Mgi Id | MGI:6116123 | Doi | 10.1080/2162402X.2017.1292195 |
| Citation | Liu H, et al. (2017) LYG1 exerts antitumor function through promoting the activation, proliferation, and function of CD4(+) T cells. Oncoimmunology 6(4):e1292195 |
| abstractText | Identification of novel stimulatory cytokines with antitumor function would have great value in tumor immunotherapy investigations. Here, we report LYG1 (Lysozyme G-like 1) identified through the strategy of Immunogenomics as a novel classical secretory protein with tumor-inhibiting function. LYG1 recombinant protein (rhLYG1) could significantly suppress the growth of B16 tumors in WT B6 mice, but not in SCID-beige mice, Rag1(-/-) mice, CD4(+)- or CD8(+) T cell-deleted mice. It could increase the number of CD4(+) and CD8(+) T cells in tumor-infiltrating lymphocytes, tumor-draining lymph nodes, and spleens, and promote IFNgamma production by T cells in tumor-bearing mice. In vitro experiments demonstrated that rhLYG1 could directly enhance IFNgamma secretion by CD4(+) T cells, but not CD8(+) T cells. Moreover, it could promote the activation, proliferation, and IFNgamma production of tumor antigen-specific CD4(+) T cells. The tumor-inhibiting effect of LYG1 was eliminated in Ifng(-/-) mice. Furthermore, LYG1 deficiency accelerated B16 and LLC1 tumor growth and inhibited the function of T cells. In summary, our findings reveal a tumor-inhibiting role for LYG1 through promoting the activation, proliferation, and function of CD4(+) T cells in antitumor immune responses, offering implications for novel tumor immunotherapy. |
