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IL-4 enhances IFN-lambda1 (IL-29) production by plasmacytoid DCs via monocyte secretion of IL-1Ra

Nicholas J Megjugorac1, Grant E Gallagher, Grant Gallagher

  • 1Humigen LLC, The Institute for Genetic Immunology, Hamilton, NJ 08690, USA.

Blood
|March 18, 2010
PubMed

Insights

Interleukin-4 (IL-4) enhances type-III interferon (IFN-lambda1) production by plasmacytoid dendritic cells (pDCs). Monocytes act as intermediaries, mediating this IL-4 effect on pDCs to regulate immune responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Type-III interferons (IFN-lambda1, IFN-lambda2, IFN-lambda3) are crucial immune modulators.
  • Plasmacytoid dendritic cells (pDCs) are key producers of IFN-lambda.
  • IFN-lambda1 inhibits T-helper 2 (Th2) responses by counteracting IL-4 effects.

Purpose of the Study:

  • To investigate whether Th2 cytokines reciprocally regulate IFN-lambda production.
  • To elucidate the cellular mechanisms underlying IL-4-mediated regulation of IFN-lambda1.

Main Methods:

  • Human peripheral lymphocytes were stimulated with IL-4.
  • IFN-lambda1 transcription and secretion were measured.
  • Depletion and reconstitution experiments identified intermediary cells.

Main Results:

  • IL-4 treatment significantly increased IFN-lambda1 transcription and secretion.
  • pDCs were not directly responsive to IL-4.
  • Monocytes, upon IL-4 stimulation, secreted IL-1 receptor antagonist (IL-Ra), which then induced IFN-lambda1 production in pDCs.

Conclusions:

  • A novel regulatory pathway for IFN-lambda1 production and pDC function was discovered.
  • Monocytes act as essential intermediaries in IL-4-driven IFN-lambda1 induction.
  • Th2 cytokines play an expanded role in immunomodulation through this pathway.

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