Regulation of immune responses by prostaglandin E2

  • Kalinski P
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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

Author-supplied keywords

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

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  • PMID: 22187483

Authors

  • P Kalinski

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