CD161 mediates prenatal immune suppression of IFN -producing PLZF+ T cells

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 t...

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Bibliographic Details
Published inbioRxiv
Main Authors Halkias, Joanna, Elze Rackaityte, Dvir Aran, Mendoza, Ventura F, Eckalbar, Walter L, Burt, Trevor D
Format Paper
LanguageEnglish
Published Cold Spring Harbor Cold Spring Harbor Laboratory Press 21.04.2018
Subjects
Adaptive immunity
Birth
Cell activation
Cytokines
Fetuses
Health risk assessment
Immune system
Immunological tolerance
Inflammation
Interferon
Intestine
Lymphocytes
Lymphocytes T
Neonates
Pregnancy
Premature birth
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Summary: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.
DOI:10.1101/305128