Fig. 4.
Factors controlling formation of different subsets of T helper cells. LXs = Lipoxins; RSvs = Resolvins; PRTs = Protectins; MaRs = Maresins. Naive CD41 T cells differentiate into 3 types of subsets of T helper cells: TH1, TH2 and TH17. TGF-β converts naive T cells into FOXP3-expressing induced Treg (iTreg) cells. T helper cell differentiation requires specific transcription factors as master regulators, which include T-bet, GATA3 and ROR-γt. Terminally differentiated T helper cells produce specific effector cytokines to bring about their distinct effector functions. TGF-β, retinoic acid or cytokines: IL-6, IL-1, IL-23, or IL-27 produced by the innate immune system’s immature or activated dendritic cells (DCs) dictate how a naive T cell develops into a FOXP31 Treg cell, a TH17 cell or otherwise. PGE2 through its receptor EP4 on T cells and dendritic cells facilitates TH1 cell differentiation and amplifies IL-23–mediated TH17 cell expansion, whereas EP4-selective antagonist inhibits TH1 and TH17 cells and suppresses autoimmune diseases. GLA, AA, EPA, DHA, lipoxins, resolvins, protectins, maresins and prostaglandins, leukotrienes and thromboxanes influence macrophage and other immunocytes’ phagocytosis, motility and ability to alter ROS generation and thus, regulate inflammation and immune response