Kaiting Yang, Yong Liang, Zhichen Sun, Longchao Liu, Jing Liao, Hairong Xu, Mingzhao Zhu, Yang-Xin Fu, Hua Peng
||Scientific Reports, 2018, Vol.8 (1), pp.1-9
||Directory of Open Access Journals
Abstract Though lymphotoxin (LT is highly expressed by type I helper T (Th1 cells, its contribution to CD4+ T cell differentiation during infections and diseases remains a mystery. In HSV-1 infection, we observed that LTβR signaling is required to limit the Th1 response. Using bone marrow chimeric mice, mixed-T-cell chimeric mice, and LTβR in vivo blockades, we unexpectedly observed that LT, especially T cell-derived LT, played an indispensable role in limiting the Th1 response. Thexa0LTβR-Ig blockade promoted the Th1 response by increasing infiltration of monocytes and monocyte-derived DCs and up-regulating IL-12xa0secretion in the lymphoid environment. Our findings identified a novel role for T cell-derived LT in manipulating Th1 differentiation.