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

Joanna Halkias, Elze Rackaityte, Dvir Aran, Ventura F Mendoza, Walter L Eckalbar, Trevor D Burt
doi: https://doi.org/10.1101/305128
Joanna Halkias
University of California, San Francisco;
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  • For correspondence: joanna.halkias@ucsf.edu
Elze Rackaityte
University of California, San Francisco;
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Dvir Aran
University of California San Francisco
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Ventura F Mendoza
University of California, San Francisco;
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Walter L Eckalbar
University of California, San Francisco;
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Trevor D Burt
University of California, San Francisco;
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Abstract

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.

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Posted April 21, 2018.
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CD161 mediates prenatal immune suppression of IFNγ-producing PLZF+ T cells
Joanna Halkias, Elze Rackaityte, Dvir Aran, Ventura F Mendoza, Walter L Eckalbar, Trevor D Burt
bioRxiv 305128; doi: https://doi.org/10.1101/305128
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CD161 mediates prenatal immune suppression of IFNγ-producing PLZF+ T cells
Joanna Halkias, Elze Rackaityte, Dvir Aran, Ventura F Mendoza, Walter L Eckalbar, Trevor D Burt
bioRxiv 305128; doi: https://doi.org/10.1101/305128

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