CD8+ T cells exhibit dual roles at the maternal-fetal interface supporting tolerance via IL-10 and TGF-β and aiding implantation and vascular remodeling through TNF-α and IFN-γ. In HIV infection, CD8+ T cells expand, driving inflammation, PD-L1 upregulation on trophoblasts, and cytotoxic dysfunction via reduced Granzyme B and Perforin, compromising placental immunity.
ABSTRACT
The global HIV epidemic presents ongoing challenges, particularly in Sub-Saharan Africa, where women of reproductive age are disproportionately affected. Despite strides in prevention strategies, maternal HIV infection continues to impact pregnancy outcomes. This review delves into the complex interplay between HIV and CD8+ T cells at the maternal-fetal interface, elucidating their roles in viral transmission and pregnancy. Maternal HIV infection introduces complexities to pregnancy, elevating the risk of adverse outcomes such as miscarriage, stillbirth, and low birth weight deliveries. The placenta, a multifunctional organ crucial for maternal–fetal exchange, serves as a site for intricate immunological interactions during HIV infection. Despite its protective mechanisms, HIV can exploit vulnerabilities, such as cell-to-cell transmission and Hofbauer cells expressing CD4 receptors, within the placenta. CD8+ T cells, as key effectors of the antiviral immune response, play a pivotal role in combating HIV within this environment. However, their precise efficacy against HIV-1 within the placenta remains unclear. This review underscores the urgent need for a comprehensive understanding of CD8+ T cell dynamics in pregnancy-related HIV infections within the placenta. Understanding the complex interactions between HIV, CD8+ T cells, and the placenta is crucial for elucidating their roles in maintaining a balanced immune response during pregnancy, thereby safeguarding the health and well-being of both mother and child.