Differential Regulation of Th1/Th2 Cytokine Responses by Placental Protein 14

Abstract

The potency of TCR signaling during primary CD4+ T cell activation influences initial cytokine expression patterns and subsequent polarization toward either Th1 or Th2 subsets. In this study, we demonstrate that the T cell inhibitor placental protein 14 (PP14; glycodelin) preferentially inhibits Th1 cytokine responses and chemokine expression when present during ex vivo priming of CD4+ T cells. PP14 synergizes with exogenously added IL-4 in skewing T cell responses. Significantly, PP14 impairs the down-regulation of GATA-3 transcriptional regulator expression that normally accompanies T cell activation, which is a prerequisite for Th1 development. Taken together, these data document for the first time the ability of PP14 to skew Th responses.

The Role of Placental Protein 14 in the Pathogenesis of Endometriosis

“…These results suggest that PP-14 secreted by ovarian endometriotic lesions may contribute to the plasma, leading to increased concentrations of PP-14 in serum of women with endometriosis. 8 Because PP-14 can inhibit natural killer (NK) cell cytotoxicity function and regulate type 1 (Th1) helper T cells and type 2 (Th2) helper T cells immune responses differently, 24,25 it is implied that PP-14 may play a role in the pathogenesis of endometriosis. 26 The PP-14 is the principal secretory phase product of endometrial epithelial cells, 27 and its serum PP-14 levels reflect endometrial cycle phase, which are in concert with progesterone levels.…”

THE ROLE OF THE DIFFERENT SUBPOPULATIONS OF CD4⁺Т LYMPHOCYTES DURING PREGNANCY

“…They have no effect on IL-4 secretion by activated T cells. Thus, they can promote Th1 proliferation inhibiting at pregnancy against the background of no negative effect on Th2 cell clonal proliferation [74,117]. PZP is a protease inhibitor of wide specify, it effects lymphocyte migration, their cytotoxic activity and secretory specifics.…”

Probiotics Applications in Autoimmune Diseases

“…Even more interestingly, gut microflora bacteria have shown ability to not only initiate an inflammatory response but also to control and inhibit such a response. Some microfloral bacteria or their metabolites can interact with the intracellular receptor TLR-9, to which the bacteria activates T cells through the production of potent anti-inflammatory cytokines such as IL-10 [117,118]. Microfloral bacteria can also produce small molecules that can enter intestinal epithelial cells to inhibit activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) [119].…”