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γδ T cells contribute to injury in the developing brain.

Artikel i vetenskaplig tidskrift
Författare Anna-Maj Albertsson
Xiaoli Zhang
Regina Vontell
Dan Bi
Roderick T Bronson
Veena Supramaniam
Ana A Baburamani
Sha Hua
Arshed Nazmi
Susanna Cardell
Changlian Zhu
Harvey Cantor
Carina Mallard
Henrik Hagberg
Jianmei W Leavenworth
Xiaoyang Wang
Publicerad i The American journal of pathology
Volym 188
Nummer/häfte 3
Sidor 757–767
ISSN 1525-2191
Publiceringsår 2018
Publicerad vid Institutionen för neurovetenskap och fysiologi
Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för kliniska vetenskaper, Avdelningen för obstetrik och gynekologi
Sidor 757–767
Språk en
Länkar dx.doi.org/10.1016/j.ajpath.2017.11...
www.ncbi.nlm.nih.gov/entrez/query.f...
Ämneskategorier Neurovetenskaper

Sammanfattning

Brain injury in premature infants, especially periventricular leukomalacia, is an important cause of neurological disabilities. Inflammation contributes to the development of perinatal brain injury, but the essential mediators leading to brain injury in early life remain largely unknown. Neonates have reduced capacity for mounting conventional αβT-cell responses. However γδT-cells are already functionally competent during early development and are important in early life immunity. We investigated the potential contribution of γδT-cells to preterm brain injury by using postmortem brains from human preterm infants with periventricular leukomalacia and two animal models of preterm brain injury-the hypoxic-ischemic mouse model and a fetal sheep asphyxia model. Large numbers of γδT-cells were observed in the brains of mice, sheep, and postmortem preterm infants after injury, and depletion of γδT-cells provided protection in the mouse model. The common γδT-cell associated cytokines interferon-γ and interleukin (IL)-17A were not detectable in the brain. Although there were increased mRNA levels of Il17f and Il22 in the mouse brains after injury, neither IL-17F nor IL-22 cytokines contributed to preterm brain injury. These findings highlight unique features of injury in the developing brain where, unlike injury in the mature brain, γδT-cells function as important initiators of injury independently of common γδT-cell associated cytokines. This new finding will help to identify therapeutic targets for preventing or treating preterm infants with brain injury.

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