Levels of Co-inhibitory Receptors (TIM-3,LAG-3 and TIGIT)in Preeclampsia Patients

T lymphocytes, as well as their regulatory subpopulations could possibly possess a part in PE . The changes in T cell subsets that may be seen in preeclampsia include low Treg activity, a shift toward Th1 responses, and the presence Th17 lymphocytes. B cells can participate in the pathophysiology of preeclampsia by producing autoantibodies against adrenoreceptors and autoantibodies that bind the AT1-R (angiotensin II type I receptor)

TH17 cells are a distinctive lineage of TCD4+ cells, which are distinguished by producing a number of effective molecules such as IL-17, which is the most important cytokine produced by these cells . IL-17 is capable of inducing the production of several cytokines, such as tumor necrosis factor alpha (TNF-α) and IL-1β which possess significant parts in PE pathophysiology .

Regulatory T lymphocytes CD4+ CD25bright are known to play an important role in the development and maintenance of tolerance in peripheral tissues . They express high level of CD25 (IL-2Ra) as well as cytotoxic T-lymphocyte antigen 4 (CTLA4) and the transcription factor Foxp3 .

It was proposed that regulatory T cells (Tregs) are responsible for mediating maternal tolerance for the fetus and their counts were found to be higher in normal pregnancies However, the role of T reg cells in the development of preeclampsia remains controversial, being decreased in some studies .) and of comparable frequencies to normal pregnancy in others (Hu et, 2008). Tregs suppress maternal immune cells through the secretion of inhibitory cytokines, such as interleukin (IL)-10 and transforming growth factor beta (TGF-β) .

systemic endothelial dysfunction, such as disturbed coagulation function, could be intensified through immune activation, resulting in inflammation and the disturbance of regulatory T (Treg) and Th17 cell balance, and contributing to further activation of the maternal immune responses .