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G-CSF drives autoinflammation in APLAID.

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Phospholipase C gamma 2-associated antibody deficiency and immune dysregulation (APLAID) is driven by granulocyte colony-stimulating factor (G-CSF). Targeting G-CSF with an antibody reversed established disease in a mouse model, offering a potential therapeutic strategy.

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Area of Science:

  • Immunology
  • Genetics
  • Molecular Biology

Background:

  • Missense mutations in PLCG2 cause autoinflammation with phospholipase C gamma 2-associated antibody deficiency and immune dysregulation (APLAID).
  • Existing treatments targeting IL-1, JAK1/2, or TNF show limited efficacy in APLAID patients.

Purpose of the Study:

  • To investigate the underlying mechanisms of APLAID and identify effective therapeutic targets.
  • To develop and validate a mouse model for APLAID research.

Main Methods:

  • Generated a mouse model with an APLAID-associated PLCG2 mutation (p.Ser707Tyr).
  • Assessed disease severity after deleting inflammasome components (caspase-1), IL-6, or TNF.
  • Analyzed cytokine profiles in mice and patients.
  • Treated APLAID mice with a G-CSF antibody.
  • Performed bone marrow transplantation experiments.

Main Results:

  • Inflammation in APLAID mice was only partially reduced by removing inflammasome function, IL-6, or TNF.
  • Elevated G-CSF levels were a key feature in both APLAID mice and patients.
  • G-CSF antibody treatment completely reversed established APLAID symptoms in mice.
  • Treatment normalized myelopoiesis, restored lymphocyte counts, and reduced G-CSF production.

Conclusions:

  • APLAID is a G-CSF-driven autoinflammatory disease.
  • Targeting G-CSF is a feasible and effective therapeutic strategy for APLAID.