Biallelic RIPK1 mutations in humans cause severe immunodeficiency, arthritis, and intestinal inflammation

Science. 2018 Aug 24;361(6404):810-813. doi: 10.1126/science.aar2641. Epub 2018 Jul 19.

Abstract

RIPK1 (receptor-interacting serine/threonine kinase 1) is a master regulator of signaling pathways leading to inflammation and cell death and is of medical interest as a drug target. We report four patients from three unrelated families with complete RIPK1 deficiency caused by rare homozygous mutations. The patients suffered from recurrent infections, early-onset inflammatory bowel disease, and progressive polyarthritis. They had immunodeficiency with lymphopenia and altered production of various cytokines revealed by whole-blood assays. In vitro, RIPK1-deficient cells showed impaired mitogen-activated protein kinase activation and cytokine secretion and were prone to necroptosis. Hematopoietic stem cell transplantation reversed cytokine production defects and resolved clinical symptoms in one patient. Thus, RIPK1 plays a critical role in the human immune system.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Arthritis / genetics*
  • Arthritis / immunology
  • Cytokines / metabolism
  • Female
  • Fibroblasts / metabolism
  • Fibroblasts / pathology
  • Humans
  • Inflammatory Bowel Diseases / genetics*
  • Inflammatory Bowel Diseases / immunology
  • Lymphopenia / genetics
  • Male
  • Mitogen-Activated Protein Kinases / metabolism
  • Pedigree
  • Receptor-Interacting Protein Serine-Threonine Kinases / genetics*
  • Severe Combined Immunodeficiency / genetics*
  • Severe Combined Immunodeficiency / immunology

Substances

  • Cytokines
  • RIPK1 protein, human
  • Receptor-Interacting Protein Serine-Threonine Kinases
  • Mitogen-Activated Protein Kinases