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Epidermal phospholipase Cδ1 regulates granulocyte counts and systemic interleukin-17 levels in mice

Kaori Kanemaru1, Yoshikazu Nakamura, Kojiro Sato

  • 1Laboratory of Genome and Biosignal, Tokyo University of Pharmacy and Life Sciences, Hachioji-shi, Tokyo 192-0392, Japan.

Nature Communications
|July 19, 2012
PubMed

Insights

Phospholipase Cδ1 deficiency in skin keratinocytes causes granulocytosis and elevates interleukin-17, mimicking inflammatory skin diseases and impacting systemic immunity.

Area of Science:

  • Biochemistry
  • Immunology
  • Dermatology

Background:

  • Phospholipase C (PLC) enzymes are crucial for phosphoinositide turnover.
  • Cellular functions of PLC are well-studied, but organ- and organism-level roles remain unclear.

Purpose of the Study:

  • To investigate the role of Phospholipase Cδ1 (PLCδ1) in vivo, particularly its functions beyond the cellular level.
  • To elucidate the connection between PLCδ1 in keratinocytes and systemic inflammatory responses.

Main Methods:

  • Generation and analysis of PLCδ1-deficient mice.
  • Conditional knockout of PLCδ1 specifically in keratinocytes.
  • Assessment of granulocytosis, cytokine levels (interleukin-17, interleukin-23), and skin pathology.
  • Analysis of human psoriatic skin and a mouse model of psoriasis.

Main Results:

  • PLCδ1-deficient mice exhibit granulocytosis and elevated serum interleukin-17.
  • Restoring PLCδ1 in keratinocytes reverses these systemic effects.
  • Conditional PLCδ1 ablation in keratinocytes recapitulates the phenotype.
  • Epidermal interleukin-17 and interleukin-23 are upregulated, linked to inflammatory skin conditions.
  • PLCδ1 is downregulated in human psoriasis and a mouse psoriasis model.

Conclusions:

  • Keratinocyte phosphoinositide turnover regulates local inflammation, systemic cytokine levels, and leukocyte counts.
  • PLCδ1 plays a critical role in maintaining immune homeostasis and preventing inflammatory skin diseases.
  • Dysregulation of PLCδ1 in keratinocytes contributes to psoriasis pathogenesis.

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