751 results match your criteria aire gene


Report of two siblings with APECED in Serbia: is there a founder effect of c.769C>T AIRE genotype?

Ital J Pediatr 2021 Jun 2;47(1):126. Epub 2021 Jun 2.

Endocrine Unit, Department of Medicine (DIMED), University of Padua, Padua, Italy.

Background: Autoimmune polyendocrinopathy-candidiasis-ectodermal-dystrophy (APECED) or autoimmune polyglandular syndrome Type 1 is a rare autosomal recessive syndrome. The disorder is caused by mutations in the AIRE (AutoImmune Regulator) gene. According to the classic criteria, clinical diagnosis requires the presence of at least two of three main components: chronic mucocutaneous candidiasis, hypoparathyroidism and primary adrenal insufficiency. Read More

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Autoimmune polyendocrine syndrome type 1: an Italian survey on 158 patients.

J Endocrinol Invest 2021 May 18. Epub 2021 May 18.

FIRS Laboratories RSR Ltd, Cardiff, UK.

Background: Autoimmune Polyglandular Syndrome type 1 (APS-1) is a rare recessive inherited disease, caused by AutoImmune Regulator (AIRE) gene mutations and characterized by three major manifestations: chronic mucocutaneous candidiasis (CMC), chronic hypoparathyroidism (CH) and Addison's disease (AD).

Methods: Autoimmune conditions and associated autoantibodies (Abs) were analyzed in 158 Italian patients (103 females and 55 males; F/M 1.9/1) at the onset and during a follow-up of 23. Read More

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Autoinmune polyendocrinopathy.

Med Clin (Barc) 2021 May 3. Epub 2021 May 3.

Departamento de Medicina Interna y Especialidades Médicas, Centre d'Atenció Integral Dos de Maig, Consorci Sanitari Integral, Barcelona, España.

Pluriglandular autoimmune syndrome (APS) can affect multiple endocrine glands and is associated with other autoimmune diseases. APS type 1 presents with hypoparathyroidism, mucocutaneous candidiasis and Addison's disease. It is caused by AutoImmune Regulator (AIRE) gene mutation. Read More

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Molecular diagnosis of childhood immune dysregulation, polyendocrinopathy, and enteropathy, and implications for clinical management.

J Allergy Clin Immunol 2021 Apr 20. Epub 2021 Apr 20.

Department of Medicine (Medical Genetics) and Department of Genome Sciences, University of Washington, Seattle, Wash. Electronic address:

Background: Most patients with childhood-onset immune dysregulation, polyendocrinopathy, and enteropathy have no genetic diagnosis for their illness. These patients may undergo empirical immunosuppressive treatment with highly variable outcomes.

Objective: We sought to determine the genetic basis of disease in patients referred with Immune dysregulation, polyendocrinopathy, enteropathy, X-linked-like (IPEX-like) disease, but with no mutation in FOXP3; then to assess consequences of genetic diagnoses for clinical management. Read More

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A distal Foxp3 enhancer enables interleukin-2 dependent thymic Treg cell lineage commitment for robust immune tolerance.

Immunity 2021 May 9;54(5):931-946.e11. Epub 2021 Apr 9.

Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. Electronic address:

Activation of the STAT5 transcription factor downstream of the Interleukin-2 receptor (IL-2R) induces expression of Foxp3, a critical step in the differentiation of regulatory T (Treg) cells. Due to the pleiotropic effects of IL-2R signaling, it is unclear how STAT5 acts directly on the Foxp3 locus to promote its expression. Here, we report that IL-2 - STAT5 signaling converged on an enhancer (CNS0) during Foxp3 induction. Read More

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Autoimmune manifestations among 461 patients with monogenic inborn errors of immunity.

Pediatr Allergy Immunol 2021 Mar 27. Epub 2021 Mar 27.

Department of Pediatrics, Hamedan University of Medical Sciences, Hamedan, Iran.

Background: The inborn errors of immunity (IEIs) are a group of heterogeneous disorders mainly characterized by severe and recurrent infections besides other complications including autoimmune and inflammatory diseases. In this study, we aim to evaluate clinical, immunologic, and molecular data of monogenic IEI patients with and without autoimmune manifestations.

Methods: We have retrospectively screened cases of monogenic IEI in the Iranian PID registry for the occurrence of autoimmunity and immune dysregulation. Read More

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Treg-associated monogenic autoimmune disorders and gut microbial dysbiosis.

Pediatr Res 2021 Mar 17. Epub 2021 Mar 17.

Department of Pediatrics, Division of Gastroenterology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA.

Primary immunodeficiency diseases (PIDs) caused by a single-gene defect generally are referred to as monogenic autoimmune disorders. For example, mutations in the transcription factor autoimmune regulator (AIRE) result in a condition called autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy; while mutations in forkhead box P3 lead to regulatory T cell (Treg)-deficiency-induced multiorgan inflammation, which in humans is called "immune dysregulation, polyendocrinopathy, enteropathy with X-linked inheritance" (or IPEX syndrome). Previous studies concluded that monogenic diseases are insensitive to commensal microbial regulation because they develop even in germ-free (GF) animals, a conclusion that has limited the number of studies determining the role of microbiota in monogenic PIDs. Read More

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AIRE deficiency, from preclinical models to human APECED disease.

Dis Model Mech 2021 Feb 5;14(2). Epub 2021 Feb 5.

Université de Nantes, Inserm, CNRS, Centre de Recherche en Transplantation et Immunologie, UMR 1064, ITUN, F-44000 Nantes, France

Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) is a rare life-threatening autoimmune disease that attacks multiple organs and has its onset in childhood. It is an inherited condition caused by a variety of mutations in the autoimmune regulator ( gene that encodes a protein whose function has been uncovered by the generation and study of -KO mice. These provided invaluable insights into the link between expression in medullary thymic epithelial cells (mTECs), and the broad spectrum of self-antigens that these cells express and present to the developing thymocytes. Read More

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February 2021

Autoimmune Addison's Disease as Part of the Autoimmune Polyglandular Syndrome Type 1: Historical Overview and Current Evidence.

Front Immunol 2021 26;12:606860. Epub 2021 Feb 26.

Section of Internal Medicine and Endocrinological and Metabolic Sciences, Department of Medicine, University of Perugia, Perugia, Italy.

The autoimmune polyglandular syndrome type 1 (APS1) is caused by pathogenic variants of the autoimmune regulator () gene, located in the chromosomal region 21q22.3. The related protein, AIRE, enhances thymic self-representation and immune self-tolerance by localization to chromatin and anchorage to multimolecular complexes involved in the initiation and post-initiation events of tissue-specific antigen-encoding gene transcription. Read More

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February 2021

Molecular pathology of thymomas: implications for diagnosis and therapy.

Virchows Arch 2021 Jan 5;478(1):101-110. Epub 2021 Mar 5.

Institute of Pathology, University Medical Centre Mannheim and Medical Faculty Mannheim, Heidelberg University, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany.

Thymomas exhibit a unique genomic landscape, comprising the lowest on average total mutational burden among adult human cancers; a unique point mutation in the GTF2I gene in WHO type A and AB thymomas (and rarely others); almost unique KMT2A-MAML2 translocations in rare WHO type B2 and B3 thymomas; a unique YAP1-MAML2 translocation in almost all metaplastic thymomas; and unique miRNA profiles in relation to GTF2I mutational status and WHO histotypes. While most thymomas can be diagnosed solely on the basis of morphological features, mutational analyses can solve challenging differential diagnostic problems. No molecular biomarkers have been identified that predict the response of unresectable thymomas to chemotherapy or agents with known molecular targets. Read More

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January 2021

Late-onset autoimmune polyendocrine syndrome type 1: a case report and literature review.

Authors:
Feixia Zhan Li Cao

Immunol Res 2021 Apr 18;69(2):139-144. Epub 2021 Feb 18.

Department of Neurology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 600 Yi Shan Road, Shanghai, 200233, China.

Autoimmune polyendocrine syndrome type 1 (APS-1), also referred to as autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), a rare monogenic disorder, is classically characterized by a triad of chronic mucocutaneous candidiasis, hypoparathyroidism, and primary adrenal insufficiency. The identified causative gene is autoimmune regulator (AIRE), which encodes a critical transcription factor and is essential for self-tolerance. Here, we describe a late-onset Chinese case who presented with symptoms of persistent tetany due to hypocalcemia. Read More

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An AIREless Breath: Pneumonitis Caused by Impaired Central Immune Tolerance.

Front Immunol 2020 27;11:609253. Epub 2021 Jan 27.

Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States.

Autoimmune-polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), a monogenic disorder caused by biallelic mutations in the gene, has historically been defined by the development of chronic mucocutaneous candidiasis together with autoimmune endocrinopathies, primarily hypoparathyroidism and adrenal insufficiency. Recent work has drawn attention to the development of life-threatening non-endocrine manifestations such as autoimmune pneumonitis, which has previously been poorly recognized and under-reported. In this review, we present the clinical, radiographic, autoantibody, and pulmonary function abnormalities associated with APECED pneumonitis, we highlight the cellular and molecular basis of the autoimmune attack in the AIRE-deficient lung, and we provide a diagnostic and a therapeutic roadmap for patients with APECED pneumonitis. Read More

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January 2021

Thymus and autoimmunity.

Semin Immunopathol 2021 02 3;43(1):45-64. Epub 2021 Feb 3.

Institute of Pathology, University Medical Centre Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167, Mannheim, Germany.

The thymus prevents autoimmune diseases through mechanisms that operate in the cortex and medulla, comprising positive and negative selection and the generation of regulatory T-cells (Tregs). Egress from the thymus through the perivascular space (PVS) to the blood is another possible checkpoint, as shown by some autoimmune/immunodeficiency syndromes. In polygenic autoimmune diseases, subtle thymic dysfunctions may compound genetic, hormonal and environmental cues. Read More

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February 2021

Thymic origins of autoimmunity-lessons from inborn errors of immunity.

Semin Immunopathol 2021 02 2;43(1):65-83. Epub 2021 Feb 2.

Division of Hematology, Oncology, Stem Cell Transplantation and Regenerative Medicine, Department of Pediatrics, Stanford University School of Medicine, Lokey Stem Cell Research Building 265 Campus Drive, West Stanford, CA, 94305, USA.

During their intrathymic development, nascent T cells are empowered to protect against pathogens and to be operative for a life-long acceptance of self. While autoreactive effector T (Teff) cell progenitors are eliminated by clonal deletion, the intrathymic mechanisms by which thymic regulatory T cell (tTreg) progenitors maintain specificity for self-antigens but escape deletion to exert their regulatory functions are less well understood. Both tTreg and Teff development and selection result from finely coordinated interactions between their clonotypic T cell receptors (TCR) and peptide/MHC complexes expressed by antigen-presenting cells, such as thymic epithelial cells and thymic dendritic cells. Read More

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February 2021

Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy in Two Siblings: Same Mutations but Very Different Phenotypes.

Genes (Basel) 2021 01 26;12(2). Epub 2021 Jan 26.

Pediatric Endocrinology Unit, Regina Margherita Children's Hospital, 10126 Turin, Italy.

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), caused by mutations in the gene, is mainly characterized by the triad of hypoparathyroidism, primary adrenocortical insufficiency and chronic mucocutaneous candidiasis, but can include many other manifestations, with no currently clear genotype-phenotype correlation. We present the clinical features of two siblings, a male and a female, with the same mutations in the gene associated with two very different phenotypes. Interestingly, the brother recently experienced COVID-19 infection with pneumonia, complicated by hypertension, hypokalemia and hypercalcemia. Read More

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January 2021

Acquired pure red cell aplasia and T cell large granular lymphocytic leukaemia in patients with autoimmune polyglandular syndrome type 1.

BMC Med Genomics 2021 Jan 19;14(1):22. Epub 2021 Jan 19.

Hematology Department, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, 100730, China.

Background: Pure red cell aplasia (PRCA) and large granular lymphocytic leukaemia (LGLL) are very rare complications of autoimmune polyendocrine syndrome type 1 (APS1). Here, we report a case of APS1 with PRCA and LGLL. Previous cases were reviewed, and possible mechanisms are discussed. Read More

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January 2021

Novel Pathogenic Variants of the AIRE Gene in Two Autoimmune Polyendocrine Syndrome Type I Cases with Atypical Presentation: Role of the NGS in Diagnostic Pathway and Review of the Literature.

Biomedicines 2020 Dec 19;8(12). Epub 2020 Dec 19.

Division of Medical Genetics, Fondazione IRCCS Casa Sollievo della Sofferenza, 71013 San Giovanni Rotondo, Italy.

. Autoimmune polyglandular syndrome type 1 (APS-1) with or without reversible metaphyseal dysplasia is a rare genetic disorder due to inactivating variants of the autoimmune regulator, gene. Clinical variability of APS-1 relates to pleiotropy, and the general dysfunction of self-tolerance to organ-specific antigens and autoimmune reactions towards peripheral tissues caused by the underlying molecular defect. Read More

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December 2020

A Patient With AIRE Mutation Who Presented With Severe Diarrhea and Lung Abscess.

Pediatr Infect Dis J 2021 01;40(1):66-69

From the Department of Pediatrics, Division of Pediatric Immunology, Hacettepe University Medical School, Ankara, Turkey.

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) (polyglandular endocrinopathy type 1) is a rare autosomal recessive disorder caused by mutations in the autoimmune regulator gene (AIRE). The major clinical features of APECED are hypoparathyroidism, adrenal insufficiency (Addison disease), and chronic mucocutaneous candidiasis. This disease is also associated with multiple other and uncommon autoimmune (autoimmune hepatitis, autoimmune enteropathy, atrophic gastritis with or without pernicious anemia, gonadal failure, diabetes mellitus, hypothyroidism, functional hyposplenism), ectodermal (alopecia and vitiligo), and inflammatory (intestinal lung disease, nephritis) features. Read More

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January 2021

Combined transient ablation and single-cell RNA-sequencing reveals the development of medullary thymic epithelial cells.

Elife 2020 11 23;9. Epub 2020 Nov 23.

Department of Genetics, Stanford University School of Medicine, Stanford, United States.

Medullary thymic epithelial cells (mTECs) play a critical role in central immune tolerance by mediating negative selection of autoreactive T cells through the collective expression of the peripheral self-antigen compartment, including tissue-specific antigens (TSAs). Recent work has shown that gene-expression patterns within the mTEC compartment are heterogenous and include multiple differentiated cell states. To further define mTEC development and medullary epithelial lineage relationships, we combined lineage tracing and recovery from transient in vivo mTEC ablation with single-cell RNA-sequencing in . Read More

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November 2020

NLRP3 Inhibition Ameliorates Severe Cutaneous Autoimmune Manifestations in a Mouse Model of Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy-Like Disease.

J Invest Dermatol 2021 Jun 11;141(6):1404-1415. Epub 2020 Nov 11.

Laboratory of Cancer Immunometabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA. Electronic address:

Patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy show diverse endocrine and nonendocrine manifestations initiated by self-reactive T cells because of AIRE mutation-induced defective central tolerance. A large number of American patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy suffer from early-onset cutaneous inflammatory lesions accompanied by an infiltration of T cells and myeloid cells. The role of myeloid cells in this setting remains to be fully investigated. Read More

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Association of AIRE (rs2075876), but not CTLA4 (rs231775) polymorphisms with systemic lupus erythematosus.

Gene 2021 Feb 26;768:145270. Epub 2020 Oct 26.

Biochemistry and Molecular Genetics Unit, Department of Basic Sciences, Faculty of Physical Therapy, Horus University - Egypt, New Damietta 34518, Egypt. Electronic address:

Background: The AIRE (rs2075876) and CTLA4 (rs231775) variants have a crucial function in controlling the negative selection and suppression of T lymphocytes. Numerous reports studied the association of AIRE and CTLA4 variants with different autoimmune disorders, but with inconclusive conclusions. The main purpose of this work is to evaluate the association of these two variants with SLE susceptibility among Egyptian patients. Read More

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February 2021

AAV9-mediated AIRE gene delivery clears circulating antibodies and tissue T-cell infiltration in a mouse model of autoimmune polyglandular syndrome type-1.

Clin Transl Immunology 2020 3;9(9):e1166. Epub 2020 Sep 3.

Department of Infection, Immunity and Cardiovascular Disease University of Sheffield Sheffield UK.

Objectives: Autoimmune polyglandular syndrome type-1 (APS-1) is a monogenic recessive disorder characterised by multiple endocrine abnormalities, chronic mucocutaneous candidiasis and high titres of serum autoantibodies. To date, no curative treatment is available; current therapies manage the symptoms rather than treating the cause and have major side effects. APS-1 is caused by mutations in the autoimmune regulator () gene. Read More

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September 2020

The Thymus in Chagas Disease: Molecular Interactions Involved in Abnormal T-Cell Migration and Differentiation.

Front Immunol 2020 2;11:1838. Epub 2020 Sep 2.

Laboratory on Thymus Research, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil.

Chagas disease, caused by the protozoan parasite , is a prevalent parasitic disease in Latin America. Presently, it is spreading around the world by human migration, thus representing a new global health issue. Chronically infected individuals reveal a dissimilar disease progression: while nearly 60% remain without apparent disease for life, 30% develop life-threatening pathologies, such as chronic chagasic cardiomyopathy (CCC) or megaviscerae. Read More

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A novel method to identify Post-Aire stages of medullary thymic epithelial cell differentiation.

Eur J Immunol 2021 02 15;51(2):311-318. Epub 2020 Sep 15.

Instituto de Investigação e Inovação em Saúde (I3S), Universidade do Porto, Porto, Portugal.

Autoimmune regulator (Aire) medullary thymic epithelial cells (mTECs) play a critical role in tolerance induction. Several studies demonstrated that Aire mTECs differentiate further into Post-Aire cells. Yet, the identification of terminal stages of mTEC maturation depends on unique fate-mapping mouse models. Read More

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February 2021

Autoimmune polyendocrine syndrome type 1 (APECED) in the Indian population: case report and review of a series of 45 patients.

J Endocrinol Invest 2021 Apr 7;44(4):661-677. Epub 2020 Aug 7.

Endocrine Unit, Department of Medicine (DIMED), University of Padua, Padua, Italy.

Background: Autoimmune polyendocrinopathy-candidiasis-ectodermal-dystrophy (APECED) or autoimmune polyglandular syndrome type 1 (APS-1) is a rare autosomal recessive genetic disease due to mutations in the AIRE (AutoImmune REgulator) gene. The clinical diagnosis is classically based on the presence of at least two of the three main components: chronic mucocutaneous candidiasis, hypoparathyroidism and primary adrenal insufficiency. Patients often suffer from other endocrine or non-endocrine autoimmune conditions throughout life. Read More

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Human Thymic Involution and Aging in Humanized Mice.

Front Immunol 2020 7;11:1399. Epub 2020 Jul 7.

Key Laboratory of Organ Regeneration & Transplantation of the Ministry of Education, The First Hospital of Jilin University, Changchun, China.

Thymic involution is an important factor leading to the aging of the immune system. Most of what we know regarding thymic aging comes from mouse models, and the nature of the thymic aging process in humans remains largely unexplored due to the lack of a model system that permits longitudinal studies of human thymic involution. In this study, we sought to explore the potential to examine human thymic involution in humanized mice, constructed by transplantation of fetal human thymus and CD34 hematopoietic stem/progenitor cells into immunodeficient mice. Read More

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Resveratrol ameliorates thymus senescence changes in D-galactose induced mice.

Microbiol Immunol 2020 Sep 27;64(9):620-629. Epub 2020 Aug 27.

Department of Histology and Embryology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, China.

The thymic microenvironment plays an important role in the development of T cells. A decrease of thymic epithelial cells is the main cause of age-related thymic atrophy or degeneration. Resveratrol (RSV), a phytoalexin produced from plants, has been shown to inhibit the adverse effects of dietary obesity on the structure and function of the thymus. Read More

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September 2020

IFN-λ Enhances Constitutive Expression of MHC Class I Molecules on Thymic Epithelial Cells.

J Immunol 2020 09 20;205(5):1268-1280. Epub 2020 Jul 20.

Institute for Research in Immunology and Cancer, University of Montreal, Montreal, Quebec H3C 3J7, Canada;

Regulation of MHC class I (MHC I) expression has been studied almost exclusively in hematolymphoid cells. We report that thymic epithelial cells (TECs), particularly the medullary TECs, constitutively express up to 100-fold more cell surface MHC I proteins than epithelial cells (ECs) from the skin, colon, and lung. Differential abundance of cell surface MHC I in primary ECs is regulated via transcription of MHC I and of genes implicated in the generation of MHC I-binding peptides. Read More

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September 2020

Delay in Diagnosis of Two Siblings with Severe Ocular Problems and Autoimmune Polyglandular Syndrome.

Iran J Allergy Asthma Immunol 2020 Jun 23;19(3):313-317. Epub 2020 Jun 23.

Department of Allergy and Clinical Immunology, Children's Medical Center Hospital, Tehran University of Medical Sciences, Tehran, Iran AND Research Center for Immunodeficiencies, Tehran University of Medical Sciences, Tehran, Iran.

Autoimmune polyendocrine syndrome type 1 (APS1) is a scarce polyendocrinopathy with autosomal recessive inheritance results from defects in the human autoimmune regulatory (AIRE) gene. In addition to three major manifestations of APS1 including mucocutaneous candidiasis, hypoparathyroidism, and Addison's disease, ophthalmic problems such as keratoconjunctivitis, dry eye, iridocyclitis, and cataract can be seen in these patients. In this article, we introduced two siblings presented with nail dystrophia, severe photophobia, and keratitis since early childhood which genetic examination revealed single nucleotide T>C translocation in their 2nd exon and heterozygous deletion mutation in their 12th exon. Read More

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Chd4 choreographs self-antigen expression for central immune tolerance.

Nat Immunol 2020 08 29;21(8):892-901. Epub 2020 Jun 29.

Department of Immunology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Autoreactive T cells are eliminated in the thymus to prevent autoimmunity by promiscuous expression of tissue-restricted self-antigens in medullary thymic epithelial cells. This expression is dependent on the transcription factor Fezf2, as well as the transcriptional regulator Aire, but the entire picture of the transcriptional program has been obscure. Here, we found that the chromatin remodeler Chd4, also called Mi-2β, plays a key role in the self-antigen expression in medullary thymic epithelial cells. Read More

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