Regulation of Immune Responses by Prostaglandin E2

By P. Kalinski. Journal of Immunology, 2012

1,418 citations recorded by the source corpus.

PGE2, an essential homeostatic factor, is also a key mediator of immunopathology in chronic infections and cancer. The impact of PGE2 reflects the balance between its cyclooxygenase 2-regulated synthesis and 15-hydroxyprostaglandin dehydrogenase-driven degradation and the pattern of expression of PGE2 receptors. PGE2 enhances its own production but suppresses acute inflammatory mediators, resulting in its predominance at late/chronic stages of immunity. PGE2 supports activation of dendritic cells but suppresses their ability to attract naive, memory, and effector T cells. PGE2 selectively suppresses effector functions of macrophages and neutrophils and the Th1-, CTL-, and NK cell-mediated type 1 immunity, but it promotes Th2, Th17, and regulatory T cell responses. PGE2 modulates chemokine production, inhibiting the attraction of proinflammatory cells while enhancing local accumulation of regulatory T cells cells and myeloid-derived suppressor cells. Targeting the production, degradation, and responsiveness to PGE2 provides tools to modulate the patterns of immunity in a wide range of diseases, from autoimmunity to cancer.

Subfields: Immunology, Oncology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/0f1651d768e328f2bd0e11187820ec69a5295b8b

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Citations in the corpus

NK Cells Stimulate Recruitment of cDC1 into the Tumor Microenvironment Promoting Cancer Immune Control (2018, background): “PGE2 likely has additional effects on NK cells, such as inducing the downregulation of NK cell activatory receptors or cytotoxic effector molecules (Kalinski, 2012).”
CD8 T Cell Exhaustion During Chronic Viral Infection and Cancer. (2019, background): “Prostaglandin E2 (PGE2) is a lipid synthesized from arachidonic acid that has a dual role as both a proinflammatory molecule (188) and an immunosuppressor and can limit immune responses (188–190).”
Cyclooxygenase-Dependent Tumor Growth through Evasion of Immunity (2015, background): “The ability to inhibit IL-12 p40 production was reminiscent of the effects of the prostanoid PGE2 (Kalinski, 2012), which we found in high amounts in CM fromBraf melanoma cells (Figure 1D).”
Autophagy, ferroptosis, pyroptosis, and necroptosis in tumor immunotherapy (2022, background): “Although the action of PGE2 and its downstream signaling has not been elaborated more detailedly, current study has provided strong evidence that PGE2 has immunosuppressive effect towards NK cells.(333) As the stimulation of ferroptosis, ROS acts a vital role in the modulation of immunity in human m”
Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal (2014, background): “IPs are a highly charged family of lipid-derived metabolites, involved in signal transduction that results in activation of Akt, mTOR [9], and calciumhomeostasis [10, 11]; (ii) sphingosine-1-phosphate, a sphingolipid derived from ceramide that is a potent messenger molecule involved in regulating ca”
Omega-3 fatty acids and inflammatory processes: from molecules to man. (2017, neutral): “Eicosanoids are important regulators and mediators of inflammatory processes [7-9] and include prostaglandins (PGs), thromboxanes and leukotrienes (LTs).”
Ferroptosis in cancer: from molecular mechanisms to therapeutic strategies (2024, background): “325,326 Overall, ferroptotic tumor cells could emit multiple immunosuppressive signals, especially DAMPs and lipid metabolites, thereby facilitating tumorigenesis and tumor growth.”