%0 Journal Article
%T ¦Ã¦Ä T Cells Contribute to Injury in the Developing Brain
%A Ana A. Baburamani
%A Anna-Maj Albertsson
%A Arshed Nazmi
%A Carina Mallard
%A Changlian Zhu
%A Dan Bi
%A Harvey Cantor
%A Henrik Hagberg
%A Regina Vontell
%A Roderick T. Bronson
%A Sha Hua
%A Susanna Cardell
%A Veena Supramaniam
%A Xiaoli Zhang
%A Xiaoyang Wang
%J Archive of "The American Journal of Pathology".
%D 2018
%R 10.1016/j.ajpath.2017.11.012
%X Brain injury in premature infants, especially periventricular leukomalacia, is an important cause of neurologic disabilities. Inflammation contributes to perinatal brain injury development, but the essential mediators that lead to early-life brain injury remain largely unknown. Neonates have reduced capacity for mounting conventional ¦Á¦ÂT-cell responses. However, ¦Ã¦ÄT cells are already functionally competent during early development and are important in early-life immunity. We investigated the potential contribution of ¦Ã¦ÄT cells to preterm brain injury using postmortem brains from human preterm infants with periventricular leukomalacia and two animal models of preterm brain injury¡ªthe hypoxic-ischemic mouse model and a fetal sheep asphyxia model. Large numbers of ¦Ã¦ÄT cells were observed in the brains of mice, sheep, and postmortem preterm infants after injury, and depletion of ¦Ã¦ÄT cells provided protection in the mouse model. The common ¦Ã¦ÄT-cell¨Cassociated cytokines interferon-¦Ã and 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, ¦Ã¦ÄT cells function as initiators of injury independently of common ¦Ã¦ÄT-cell¨Cassociated cytokines. This finding will help to identify therapeutic targets for preventing or treating preterm infants with brain injury
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5840494/