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Jak3 deficiency blocks innate lymphoid cell development.

M L Robinette1, M Cella1, J B Telliez2

  • 1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA.

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|May 18, 2017
PubMed
Summary
This summary is machine-generated.

Mutations in Janus kinase 3 (JAK3) cause severe combined immunodeficiency (SCID). JAK inhibitors, like tofacitinib, impact innate lymphoid cells (ILCs), potentially explaining their therapeutic effects in immune conditions.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Loss-of-function mutations in Janus kinase 3 (JAK3) lead to autosomal recessive severe combined immunodeficiency (SCID), primarily affecting the immune system.
  • This understanding has driven the development of JAK inhibitors for immunosuppressive therapies.
  • Innate lymphoid cells (ILCs) are crucial for innate immunity and cytokine production.

Purpose of the Study:

  • To investigate the role of JAK3 in innate lymphoid cell (ILC) development and function.
  • To determine the impact of JAK inhibitors on ILCs, particularly in the context of potential therapeutic applications.

Main Methods:

  • Characterization of a spontaneous Jak3 mutation in the B6.Cg-Nr1d1tm1Ven/LazJ mouse model exhibiting SCID.
  • Assessment of ILC differentiation and cytokine production in Jak3-deficient mice and human ILCs.
  • In vitro studies using JAK inhibitors (tofacitinib and PF-06651600) on human intraepithelial ILC1 (iILC1) and ILC3 cells.

Main Results:

  • A spontaneous Jak3 mutation in mice resulted in a SCID phenotype and impaired innate lymphoid cell (ILC) generation.
  • JAK3 deficiency blocked ILC differentiation at precursor stages in the bone marrow.
  • JAK inhibitors (tofacitinib and PF-06651600) reduced IFN-γ production by iILC1s, impaired iILC1 and ILC3 proliferation, and affected human ILC differentiation in vitro.

Conclusions:

  • JAK3 is essential for the development of antigen-independent innate lymphoid cells (ILCs).
  • Therapeutic inhibition of JAK signaling pathways impacts ILC function and proliferation.
  • These findings suggest that JAK inhibitor efficacy in immune-mediated conditions may be partly mediated through effects on ILCs.