T cell-derived lymphotoxin limits Th1 response during HSV-1 infection

Kaiting Yang, Yong Liang, Zhichen Sun, Longchao Liu, Jing Liao, Hairong Xu, Mingzhao Zhu, Yang-Xin Fu, Hua Peng

Research output: Contribution to journalArticlepeer-review

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. The LTβR-Ig blockade promoted the Th1 response by increasing infiltration of monocytes and monocyte-derived DCs and up-regulating IL-12 secretion in the lymphoid environment. Our findings identified a novel role for T cell-derived LT in manipulating Th1 differentiation.

Original languageEnglish (US)
Article number17727
JournalScientific reports
Volume8
Issue number1
DOIs
StatePublished - Dec 1 2018

ASJC Scopus subject areas

  • General

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