Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The immunological and genetic basis of immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome.

Current opinion in allergy and clinical immunology - 1 Dec 2015

Bin Dhuban Khalid, Piccirillo Ciriaco A

Abstract excerpt

PURPOSE OF REVIEW: This article presents a comprehensive review of the immunodysregulation, polyendocrinopathy, enteropathy and X-linked (IPEX) syndrome, covering both the clinical and molecular aspects of the disease. (Figure is included in full-text article.) RECENT FINDINGS: The IPEX syndrome is a rare immunological disorder in humans caused by inheritable mutations in the FOXP3 gene, the master...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Lineage
Share to Diarrhea
Share to Forkhead Transcription Factors

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Genetic Diseases, X-Linked

Share to Homeostasis

Share to Immune System Diseases

Share to Self Tolerance

Share to T-Lymphocytes, Regulatory

Source

Identifiers

PMID: 26485097
DOI: 10.1097/ACI.0000000000000214

Genes

FOXP3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The immunological and genetic basis of immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome.PMID 26485097Read ↗

Immune dysregulation, polyendocrinopathy, enteropathy, and X-linked inheritance (IPEX), a syndrome of systemic autoimmunity caused by mutations of FOXP3, a critical regulator of T-cell homeostasis.Semantic proximity Read ↗

Immune dysregulation, polyendocrinopathy, enteropathy, X-linked: forkhead box protein 3 mutations and lack of regulatory T cells.Semantic proximity Read ↗

Molecular feature and therapeutic perspectives of immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome.Semantic proximity Read ↗

Immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) and IPEX-related disorders: an evolving web of heritable autoimmune diseases.Semantic proximity Read ↗

From IPEX syndrome to FOXP3 mutation: a lesson on immune dysregulation.Semantic proximity Read ↗

Immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome: A systematic review.Semantic proximity Read ↗

Mechanistic associations of a mild phenotype of immunodysregulation, polyendocrinopathy, enteropathy, x-linked syndrome.Semantic proximity Read ↗

The immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) is caused by mutations of FOXP3.Semantic proximity Read ↗

Clinical and immunological characteristics of five patients with immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome in China-expanding the atypical phenotypes.Semantic proximity Read ↗

Clinical and molecular profile of a new series of patients with immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome: inconsistent correlation between forkhead box protein 3 expression and disease severity.Semantic proximity Read ↗

Immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) associated with pemphigoid nodularis: a case report and review of the literature.Semantic proximity Read ↗

FOXP3 deficiency, from the mechanisms of the disease to curative strategies.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.