RT Journal Article
SR Electronic
T1 CD161 mediates prenatal immune suppression of IFNγ-producing PLZF<sup>+</sup> T cells
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 305128
DO 10.1101/305128
A1 Joanna Halkias
A1 Elze Rackaityte
A1 Dvir Aran
A1 Ventura F. Mendoza
A1 Walter L. Eckalbar
A1 Trevor Burt
YR 2018
UL http://biorxiv.org/content/early/2018/04/21/305128.abstract
AB While the fetal immune system defaults to a program of tolerance, there is concurrent need for protective immunity to meet the antigenic challenges after birth. Activation of fetal T cells is associated with fetal inflammation and the termination of pregnancy, yet which fetal T cells contribute to this process is poorly understood. Here we show a transcriptionally distinct population of pro-inflammatory T cells that predominates in the human fetal intestine. Activation of PLZF+ T cells results in rapid production of Th1 cytokines and is inhibited upon ligation of surface CD161. This mechanism of fetal immune suppression may inform how immune dysregulation could result in fetal and neonatal inflammatory pathologies such as preterm birth. Our data support that human development of protective adaptive immunity originates in utero within the specialized microenvironment of the fetal intestine.