A human IFNGR1 small deletion hotspot associated with dominant susceptibility to mycobacterial infection

Nat Genet. 1999 Apr;21(4):370-8. doi: 10.1038/7701.

Abstract

The immunogenetic basis of severe infections caused by bacille Calmette-Guérin vaccine and environmental mycobacteria in humans remains largely unknown. We describe 18 patients from several generations of 12 unrelated families who were heterozygous for 1 to 5 overlapping IFNGR1 frameshift small deletions and a wild-type IFNGR1 allele. There were 12 independent mutation events at a single mutation site, defining a small deletion hotspot. Neighbouring sequence analysis favours a small deletion model of slipped mispairing events during replication. The mutant alleles encode cell-surface IFNgamma receptors that lack the intra-cytoplasmic domain, which, through a combination of impaired recycling, abrogated signalling and normal binding to IFNgamma exert a dominant-negative effect. We thus report a hotspot for human IFNGR1 small deletions that confer dominant susceptibility to infections caused by poorly virulent mycobacteria.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / metabolism
  • BCG Vaccine / adverse effects
  • BCG Vaccine / therapeutic use
  • DNA-Binding Proteins / metabolism
  • Female
  • Fibroblasts / drug effects
  • Fibroblasts / immunology
  • Gene Expression
  • Genetic Predisposition to Disease / genetics*
  • Genetic Predisposition to Disease / immunology
  • Heterozygote
  • Humans
  • Interferon gamma Receptor
  • Interferon-gamma / pharmacology
  • Male
  • Mycobacterium / pathogenicity
  • Mycobacterium Infections / genetics
  • Mycobacterium Infections / immunology*
  • Pedigree
  • RNA, Messenger / metabolism
  • Receptors, Interferon / genetics*
  • Receptors, Interferon / metabolism
  • STAT1 Transcription Factor
  • Sequence Deletion*
  • Trans-Activators / metabolism
  • Transfection

Substances

  • BCG Vaccine
  • DNA-Binding Proteins
  • RNA, Messenger
  • Receptors, Interferon
  • STAT1 Transcription Factor
  • STAT1 protein, human
  • Trans-Activators
  • Interferon-gamma