PGI2 as a regulator of CD4+ subset differentiation and function

Abstract

Prostaglandin (PG)I2 has important regulatory functions on the innate and adaptive immune systems. Recent experimental evidence reveals that PGI2 modulates the development and function of CD4+ T cells subsets, including Th1, Th2, and Th17 cell responses. In vitro and in vivo studies support that PGI2 generally has an inhibitory effect on Th1 and Th2 activation, differentiation, and cytokine production. In contrast, PGI2 seems to enhance Th17-favoring polarization conditions, resulting in Th17 cytokine production. Therefore, PGI2 may either promote or inhibit individual CD4+ cell subsets and impact adaptive immune responses.

Nano-LC-MS/MS for the quantitation of prostanoids in immune cells

“…To list very briefly a few examples of their manifold effects, PGE 2 is known to induce fever, pain, and inflammation [4], whereas PGD 2 is involved in allergic reactions [5]. PGF 2α was discovered to regulate the cytokine response of mast cells [6], while PGI 2 is known to modulate immune cell functions, for example of T helper cells [7]. Finally, TXA 2 is produced in platelets, activated macrophages, monocytes, and dendritic cells and has proinflammatory functions [3].…”

“…T cells are key players in cell-mediated immunity, and type IV hypersensitivity reactions are generally T cellmediated [39]. There are diverse subsets, two of them are the T helper cells (CD4 + T cells) which support and regulate the immune response [7] and the cytotoxic T cells (CD8 + T cells), which destroy infected cells or tumor cells [40]. We used our method for quantitation of the prostanoid production of CD4 + and CD8 + T lymphocytes from untreated control mice, nonsensitized mice treated with oxazolone, and mice that had been sensitized with oxazolone and were treated again.…”

Effect of treatment with epoprostenol and endothelin receptor antagonists on the development of thyrotoxicosis in patients with pulmonary arterial hypertension

“…The T-helper 17 (Th17)-interleukin (IL)-17 axis plays important roles in the pathogenesis of autoimmune disease. Prostacyclin accelerates the differentiation of naïve T cells into Th17 cells and enhances Th17 cell function [13,14], endothelin increases the production of IL-17 from Th17 cells [15,16], and PDE5 accelerates the differentiation of naïve T cells into Th17 cells [17]. Thus, prostacyclin analogues may accelerate the development of autoimmune diseases, whereas inhibitors of endothelin and PDE5 may prevent the development of autoimmune diseases.…”

Prostanoids in allergy

“…In in-vitro studies, PGE 2 drives Ig class switching to IgE by exert important roles in cutaneous immune response and might play significant roles in AD. PGI 2 -IP signaling on naive CD4 + T cells facilitates Th1 differentiation in CHS47 , although the role of PGI 2 in Th1/2 differentiation is context-dependent48 . Cutaneous DCs produce abundant TXA 2 , which acts on naïve T cells to impair the DC-T cell interaction and negatively regulates the priming of T cells49 .…”