Bisphenol A in combination with TNF-alpha selectively induces Th2 cell-promoting dendritic cells in vitro with an estrogen-like activity.

Bisphenol A (BPA) is a monomer used in manufacturing a wide range of chemical products, including epoxy resins and polycarbonate. BPA, an important endocrine disrupting chemical that exerts estrogen-like activities, is detectable at nanomolar levels in human serum worldwide. The pregnancy associated doses of 17beta-estradiol (E2) plus tumor-necrosis factor-alpha (TNF-alpha) induce distorted maturation of human dendritic cells (DCs) that result in an increased capacity to induce T helper (Th) 2 responses.

Cytokine-dependent modification of IL-12p70 and IL-23 balance in dendritic cells by ligand activation of Valpha24 invariant NKT cells.

CD1d-restricted invariant NKT (iNKT) cells play crucial roles in various types of immune responses, including autoimmune diseases, infectious diseases and tumor surveillance. The mechanisms underlying their adjuvant functions are well understood. Nevertheless, although IL-4 and IL-10 production characterize iNKT cells able to prevent or ameliorate some autoimmune diseases and inflammatory conditions, the precise mechanisms by which iNKT cells exert immune regulatory function remain elusive.

17 Beta-estradiol (E2) plus tumor necrosis factor-alpha induces a distorted maturation of human monocyte-derived dendritic cells and promotes their capacity to initiate T-helper 2 responses.

There is growing evidence that 17 beta-estradiol (E2) modulates immune function. Recent studies indicated that certain effects of E2 on in vivo immune function are not a result of a direct action on T cells, but rather an indirect action on antigen-presenting cells. This study demonstrates that the pregnancy-associated doses of E2 plus tumor necrosis factor-alpha (TauNuF alpha) induce distorted maturation of human dendritic cells (DCs) that result in an increased capacity to induce T helper (Th) 2 responses.

Distinct subsets of human invariant NKT cells differentially regulate T helper responses via dendritic cells.

Invariant natural killer T (iNKT) cells regulate the T helper (Th) 1/2 balance and elicit either enhancement or suppression of the immune responses. However, the exact mechanism by which iNKT cells exert these contrasting functions has remained elusive. We demonstrate herein that two major distinct subsets of human iNKT cells, CD4+CD8beta(-) (CD4+) and CD4(-)CD8beta(-) (double negative; DN) cells, express functional CD40 ligand (CD40L), but they differentially regulate the dendritic cell (DC) function by reciprocal NKT-DC interactions, thereby influencing the subsequent Th response.

Role of human non-invariant NKT lymphocytes in the maintenance of type 2 T helper environment during pregnancy.

The molecular and cellular mechanisms that generate the T(h)2 cytokine environment necessary for the maintenance of pregnancy are still not fully understood. We herein show that the human decidua is highly enriched for TCR alpha beta(+)CD161(+) NKT cells. They express non-invariant antigen receptors encoded by diverse TCRV alpha- and V beta-chain gene segments, thereby referred to as non-invariant NKT (non-iNKT) cells.

Identification of functional type 1 ryanodine receptors in human dendritic cells.

Ryanodine receptor (RyR) is a Ca(2+) channel that mediates Ca(2+) release from intracellular stores. Altered Ca(2+) homeostasis in skeletal muscle which usually occurs as a result of point mutations in type 1 RyR1 (RyR1) is a key molecular event triggering malignant hyperthermia (MH). There are three RyR isoforms, and we herein show, for the first time, that human dendritic cells (DCs) preferentially express RyR1 mRNA among them.

[Propofol suppresses the responses in hypoglossal nerve activity to hypercapnic-hypoxic stimulation].

Background: Upper airway obstruction and inadequate ventilation often arise during sedation and anesthesia by propofol. To estimate the influence of propofol (PP) on respiratory control, we studied its effect on the neural activity and the respiratory response caused by a brief (60 sec) respiratory arrest (RA) manifesting in the hypoglossal nerve (HG) and the phrenic nerve (PN) in rabbits.

Methods: Experiments were performed on adult rabbits vagotomized, paralyzed and ventilated artificially with 50% N2O, 50% oxygen and 0.