Placental malaria-associated suppression of parasite-specific immune response in neonates has no major impact on systemic CD4 T cell homeostasis

2011

Article référencé dans le Web of Science WOS:000291788700032

Soulard V., Zin M. A., Fitting C., Ibitokou S., Oesterholt M., Luty A. J. F., Perrin R. X., Massougbodji A., Deloron Philippe, Bandeira A., Fievet Nadine

Infection and Immunity, 2011, 79 (7), p. 2801-2809 ISSN 0019-9567

In areas where Plasmodium falciparum is endemic, pregnancy is associated with accumulation of infected red blood cells (RBCs) in the placenta, a condition referred to as placental malaria (PM). Infants born to PM-positive mothers are at an increased risk of malaria, which is putatively related to the transplacental passage of parasite-derived antigens, with consequent tolerization of the fetal immune system. Here we addressed the impact of PM on the regulation of neonatal T cell responses. We found that the frequency of regulatory CD25(+) CD127(-/low) Foxp3(+) CD4(+) T cells was significantly decreased in neonates born to mothers with high levels of P. falciparum-induced placental inflammation, consisting mainly of primigravid mothers. However, at the individual level, the ratio between regulatory and effector (CD25(+) CD127(+) Foxp3(-)) CD4(+) T cells was unaffected by PM. In addition, parasite-induced CD4(+) T cell activation and production of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and IL-10 were strongly reduced in neonates born to PM-positive mothers. Thus, our results show that active PM at delivery is associated with a marked suppression of P. falciparum-specific cellular neonatal immune responses, affecting secretion of both pro-and anti-inflammatory cytokines. Additionally, our results suggest that, as in adults, effector and regulatory CD4(+) T cell populations are tightly coregulated in all neonates, irrespective of the maternal infection status.

Entomologie médicale / Parasitologie / Virologie [052]

Fonds IRD [F B010087126]

fdi:010087126