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AIRE

autoimmune regulator

The AIRE gene encodes the autoimmune regulator protein, which plays a critical role in the development and function of the immune system by preventing autoimmune reactions. The AIRE gene provides instructions for producing the autoimmune regulator protein, primarily active in the thymus.

Chromosome 21q22.3 Autosomal recessive HGNC:360 Tier C
AIRE 21q22.3 p arm q arm 21

AIRE is located on the long (q) arm of chromosome 21, at band 21q22.3. Arm ratio per GRCh38 - banding schematic.

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Overview

The AIRE gene, or autoimmune regulator, is fundamental to immune system function, particularly in the thymus. Its encoded protein is crucial for immune self-tolerance, helping T cells to recognise and avoid attacking the body's own cells and tissues [PMID:33676228]. Dysfunction of the AIRE gene can lead to autoimmune conditions where the immune system mistakenly targets the body's own organs [PMID:29665510].

What the gene does

The AIRE protein is predominantly active within the thymus, an organ vital for immune system development. Here, it facilitates the 'thymic education' of T cells, which are a type of immune cell. This process ensures that T cells learn to differentiate between endogenous proteins and foreign pathogens. The autoimmune regulator protein achieves this by promoting the expression of a wide array of self-antigens in the thymus. T cells that react strongly to these self-antigens are typically eliminated, preventing them from causing autoimmune damage [PMID:29665510]. This mechanism is critical for establishing central immune tolerance, ensuring the immune system only targets harmful invaders while sparing healthy bodily tissues.

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Chromosome location

The AIRE gene is situated on chromosome 21 at position 21q22.3. This specific location on the long arm of chromosome 21 houses the genetic information necessary for producing the autoimmune regulator protein.

Protein structure

The AIRE protein consists of 545 amino acids and features several distinct domains and motifs. It contains an N-terminal HSR domain (amino acids 1-105) and two PHD-type zinc fingers: PHD-type 1 (amino acids 296-343) and PHD-type 2 (amino acids 434-475). There are also several LXXLL motifs, including LXXLL motif 1 (amino acids 7-11), LXXLL motif 2 (amino acids 63-67), LXXLL motif 3 (amino acids 414-418), and LXXLL motif 4 (amino acids 516-520). Disordered regions are found at amino acids 101-178, 234-290, 348-382, and 489-508. Additionally, specific regions (amino acids 295-298, 304-312, and 331-335) are involved in interaction with histone H3 not methylated at 'Lys-4'. The SAND domain is located between amino acids 181-280.

Domain map · 545 amino acids
HSR (1–105)LXXLL motif 1 (7–11)LXXLL motif 2 (63–67)SAND (181–280)PHD-type 1 (296–343)LXXLL motif 3 (414–418)PHD-type 2 (434–475)LXXLL motif 4 (516–520)HSR1–105SAND181–280PHD-type 1296–3431~273545
Domain - independent functional unit
Motif - short conserved sequence
Zinc finger - zinc-binding structural motif
🧬 Explore 3D structure on AlphaFold
UniProt:O43918Length:545 aaStructure:AlphaFold

Key variants

Variants within the AIRE gene can lead to altered protein function, which may impair the immune system's ability to maintain self-tolerance. These genetic changes can affect the various domains and motifs crucial for the protein's proper action, potentially disrupting T cell education in the thymus. Most known pathogenic variants are associated with an autosomal recessive inheritance pattern.

The table below shows the top 10 pathogenic or likely-pathogenic variants currently classified in ClinVar for AIRE.
View all on ClinVar →

Sample of pathogenic variants

10 pathogenic / likely-pathogenic variants from ClinVar, ranked by review status (expert-panel-reviewed first). This is a sample; recurrent founder variants in a specific population may not appear here - see the full ClinVar listing via the link above.

Variant (HGVS) Protein change Classification Evidence Associated condition
c.1045C>T
single nucleotide variant
p.Gln349Ter Pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1
c.1233del
Deletion
p.Ser412fs Pathogenic/Likely pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1
c.1235del
Deletion
p.Ser412fs Pathogenic/Likely pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1
c.1311C>A
single nucleotide variant
p.Cys437Ter Pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1
c.1347C>A
single nucleotide variant
p.Cys449Ter Pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1
c.173C>G
single nucleotide variant
p.Ala58Gly Pathogenic/Likely pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1
c.195G>A
single nucleotide variant
p.Trp65Ter Pathogenic/Likely pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1
c.349del
Deletion
p.Ala117fs Pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1
c.449del
Deletion
p.Gly150fs Pathogenic/Likely pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1
c.510_522del
Deletion
p.Glu171fs Pathogenic/Likely pathogenic ★★☆☆ Polyglandular autoimmune syndrome, type 1

Evidence stars indicate ClinVar review status. Individual variant interpretation should always be performed by a qualified clinical laboratory - many variants remain classified as Variants of Uncertain Significance (VUS) pending more research.

Associated conditions

Pathogenic variants in the AIRE gene are primarily associated with Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy (APECED), also known as Autoimmune Polyendocrine Syndrome type 1 (APS type 1). APECED is an inherited condition characterised by a combination of endocrine gland deficiencies, chronic mucocutaneous candidiasis, and ectodermal dystrophies, all stemming from immune system dysregulation [PMID:29665510].

Inheritance pattern

Conditions caused by pathogenic AIRE variants typically follow autosomal recessive inheritance.

Carrier parent 1 altered copy Carrier parent 1 altered copy Affected Carrier Carrier Unaffected Affected Carrier Unaffected Circles = females · Squares = males

When both parents are carriers, each child has a 25% chance of being affected, 50% of being a carrier, and 25% of being unaffected.

Carrier frequency by population How common is heterozygous AIRE carrier status across ancestry groups?

UK clinical status

The AIRE gene is included in several UK NHS national genomic testing panels. It is part of panels for Autoimmune Polyendocrinopathy Syndrome (R155), Congenital adrenal hypoplasia (R150), Familial hypoparathyroidism (R153), and Primary immunodeficiency or monogenic inflammatory bowel disease (R15). It is also listed on panels for COVID-19 research, DDG2P, Multi-organ autoimmune diabetes, Rare genetic inflammatory skin disorders (R332), and Retinal disorders (R32).

Frequently asked questions

What is the main role of the AIRE gene?

The AIRE gene provides instructions for the autoimmune regulator protein, which is critical for preventing the immune system from attacking the body's own tissues. It helps T cells in the thymus learn to distinguish between self and non-self proteins.

What condition is most commonly associated with AIRE gene variants?

Variants in the AIRE gene are most commonly associated with Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy (APECED), also known as Autoimmune Polyendocrine Syndrome type 1 (APS type 1).

How is APECED inherited?

APECED is inherited in an autosomal recessive pattern, meaning an individual must inherit two copies of the altered AIRE gene (one from each parent) to develop the condition.

References

  1. Anderson MS, Su MA. AIRE expands: new roles in immune tolerance and beyond. Nature reviews. Immunology. 2016. PMID: 26972725
  2. Ferre EM, Rose SR, Rosenzweig SD. Redefined clinical features and diagnostic criteria in autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy. JCI insight. 2016. PMID: 27588307
  3. De Martino L, Capalbo D, Improda N. Novel Findings into AIRE Genetics and Functioning: Clinical Implications. Frontiers in pediatrics. 2016. PMID: 27597936
  4. Kisand K, Peterson P. Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy. Journal of clinical immunology. 2015. PMID: 26141571
  5. Gallo V, Giardino G, Capalbo D. Alterations of the autoimmune regulator transcription factor and failure of central tolerance: APECED as a model. Expert review of clinical immunology. 2013. PMID: 23256763
  6. Laan M, Peterson P. The many faces of aire in central tolerance. Frontiers in immunology. 2013. PMID: 24130560
  7. De Martino L, Capalbo D, Improda N. APECED: A Paradigm of Complex Interactions between Genetic Background and Susceptibility Factors. Frontiers in immunology. 2013. PMID: 24167503
  8. Puel A, Döffinger R, Natividad A. Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I. The Journal of experimental medicine. 2010. PMID: 20123958
  9. Kisand K, Bøe Wolff AS, Podkrajsek KT. Chronic mucocutaneous candidiasis in APECED or thymoma patients correlates with autoimmunity to Th17-associated cytokines. The Journal of experimental medicine. 2010. PMID: 20123959
Educational content. This page is not medical or genetic advice, is not individually reviewed by a clinician for each reader, and should not replace a consultation with a qualified healthcare professional or genetic counsellor. If you are considering genetic testing or acting on a test result, book a consultation.
Data sources Last updated 6 September 2026. Content compiled from HGNC · MedlinePlus Genetics · ClinGen · Genomics England PanelApp · NHS National Genomic Test Directory · ClinVar · UniProt · AlphaFold .