Human Congenital Infection With Trypanosoma cruzi Induces Phenotypic and Functional Modifications of Cord Blood NK Cells

Emmanuel Hermann, Cristina Alonso-Vega, Aurelie Berthe, Carine Truyens, Amilcar Flores, Marisol Cordova, Lorenzo Moretta, Faustino Torrico, Veronique Braud, Yves Carlier
<span title="">2006</span> <i title="Springer Nature"> <a target="_blank" rel="noopener" href="https://fatcat.wiki/container/whvfa7dwcjdv3htgapecctdu2q" style="color: black;">Pediatric Research</a> </i> &nbsp;
We studied the phenotype and activity of cord blood natural killer (NK) cells in newborns congenitally infected with Trypanosoma cruzi. We found that the proportion of CD56 bright NK cells was significantly decreased in cord blood from these newborns, suggesting they may have been recruited to secondary lymphoid organs. The remaining CD56 bright NK cells exhibited a defective ability in the production of interferon (IFN)-␥ following in vitro activation with interleukin (IL)-12 ϩ IL-2 or IL-12 ϩ
more &raquo; ... IL-15 cytokines, as compared with NK cells from uninfected newborns. In addition, cord blood NK cells from congenitally infected newborns stimulated with cytokines have a decreased release of granzyme B (GrB) when incubated with K562 target cells. This defect in cytotoxic effector function is associated with a reduced surface expression of activating NK receptors (NKp30, NKp46, and NKG2D) on CD56 dim NK cells compared with uninfected newborns. These alterations of fetal NK cells from congenitally infected newborns may reflect a down-regulation of the NK cell response after an initial peak of activation and could also be the result of T. cruzi modulating the immune response. (Pediatr Res 60: 38-43, 2006)
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