FOXP3 deficiency, from the mechanisms of the disease to curative strategies

Immunol Rev. 2024 Mar;322(1):244-258. doi: 10.1111/imr.13289. Epub 2023 Nov 23.

Abstract

FOXP3 gene is a key transcription factor driving immune tolerance and its deficiency causes immune dysregulation, polyendocrinopathy, enteropathy X-linked syndrome (IPEX), a prototypic primary immune regulatory disorder (PIRD) with defective regulatory T (Treg) cells. Although life-threatening, the increased awareness and early diagnosis have contributed to improved control of the disease. IPEX currently comprises a broad spectrum of clinical autoimmune manifestations from severe early onset organ involvement to moderate, recurrent manifestations. This review focuses on the mechanistic advancements that, since the IPEX discovery in early 2000, have informed the role of the human FOXP3+ Treg cells in controlling peripheral tolerance and shaping the overall immune landscape of IPEX patients and carrier mothers, contributing to defining new treatments.

Keywords: IPEX; TSDR; Treg cells; autoreactive B cells; autoreactive T cells; gene therapy.

Publication types

  • Review

MeSH terms

  • Forkhead Transcription Factors / genetics
  • Genetic Diseases, X-Linked* / genetics
  • Genetic Diseases, X-Linked* / therapy
  • Humans
  • Immune System Diseases* / genetics
  • Immune System Diseases* / therapy
  • Intestinal Diseases* / genetics
  • Mutation
  • Polyendocrinopathies, Autoimmune* / genetics
  • Syndrome
  • T-Lymphocytes, Regulatory

Substances

  • Forkhead Transcription Factors
  • FOXP3 protein, human