Maternal chronic inflammation (MI) can adversely affect offspring's immune development resulting in dysregulation of splenic T cells. Interleukin 1 beta (IL‐1β) contributes to mediating inflammation in the placenta to induce… Click to show full abstract
Maternal chronic inflammation (MI) can adversely affect offspring's immune development resulting in dysregulation of splenic T cells. Interleukin 1 beta (IL‐1β) contributes to mediating inflammation in the placenta to induce fetal toxicity and cause long‐term postnatal sequelae. In this study, we investigated how MI affects the T‐cell immune development from the fetal to the neonatal period and how offspring responded to postnatal IL‐1β challenge when exposed to an adverse intrauterine environment. We also extend these studies to examine the sex‐specific differences.
               
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