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      Regulation of immune responses by prostaglandin E2.

      The Journal of Immunology Author Choice

      metabolism, immunology, Neoplasms, Killer Cells, Natural, Inflammation Mediators, physiology, Immunologic Memory, Humans, Dinoprostone, Dendritic Cells, Cyclooxygenase 2, Chemokines, CD4-Positive T-Lymphocytes, Autoimmune Diseases, Animals

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          Abstract

          PGE(2), an essential homeostatic factor, is also a key mediator of immunopathology in chronic infections and cancer. The impact of PGE(2) reflects the balance between its cyclooxygenase 2-regulated synthesis and 15-hydroxyprostaglandin dehydrogenase-driven degradation and the pattern of expression of PGE(2) receptors. PGE(2) enhances its own production but suppresses acute inflammatory mediators, resulting in its predominance at late/chronic stages of immunity. PGE(2) supports activation of dendritic cells but suppresses their ability to attract naive, memory, and effector T cells. PGE(2) 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. PGE(2) 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 PGE(2) provides tools to modulate the patterns of immunity in a wide range of diseases, from autoimmunity to cancer.

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          Author and article information

          Journal
          22187483
          3249979
          10.4049/jimmunol.1101029

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