Abdulwahab Elsayed

Medizinische Hochschule Hannover

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Faranaz Atschekzei

Medizinische Hochschule Hannover

Georgios Sogkas

Medizinische Hochschule Hannover

Theresa Graalmann

Medizinische Hochschule Hannover

Sandra von Hardenberg

Medizinische Hochschule Hannover

Felix C. Ringshausen

Medizinische Hochschule Hannover

Torsten Witte

Medizinische Hochschule Hannover

Thea Thiele

Medizinische Hochschule Hannover

Gunnar Schmidt

Medizinische Hochschule Hannover

Mykola Fedchenko

Medizinische Hochschule Hannover

Diana Ernst

Medizinische Hochschule Hannover

Cooperative Institutions

Medizinische Hochschule Hannover

German Center for Infection Research

German Center for Lung Research

Center for Rheumatology

University of Freiburg

University Medical Center Freiburg

University of Göttingen

Heinrich Heine University Düsseldorf

Düsseldorf University Hospital

Tehran University of Medical Sciences

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Phenotypic and pathomechanistic overlap between tapasin and TAP deficiencies

Journal of Allergy and Clinical Immunology (2024)

Abdulwahab Elsayed Sandra von Hardenberg Faranaz Atschekzei Theresa Graalmann Christine Jänke

BackgroundHuman tapasin deficiency is reported to cause an autosomal-recessive inborn error of immunity characterized by substantially reduced cell surface expression of major histocompatibility complex class I (MHC-I).ObjectiveWe evaluated the immunologic and clinical consequences of tapasin deficiency.MethodsA novel homozygous variant in TAPBP was identified by means of whole genome sequencing. The expression of tapasin and both subunits of the transporter associated with antigen presentation (TAP) were evaluated by Western blot analysis. Cell surface and intracellular expression of MHC-I were evaluated by flow cytometry. Small interfering RNAs were used for silencing TAPBP expression in HEK293T cells.ResultsWe identified a deletion in TAPBP (c.312del, p.(K104Nfs∗6)) causing tapasin deficiency in a patient with bronchiectasis and recurrent respiratory tract infections as well as herpes zoster. Besides substantial reduction in TAP1 and TAP2 expression, peripheral blood mononuclear cells from this patient and TAPBP-knockdown HEK293T cells, displayed reduced cell surface expression of MHC-I, while reduction in intracellular expression of MHC-I was less prominent, suggesting a defect in MHC-I trafficking to the plasma membrane. IFN-α improved cell surface expression of MHC-I in tapasin deficient lymphocytes and TAPBP-knockdown HEK293T cells, representing a possible therapeutic approach for tapasin deficiency.ConclusionTapasin deficiency is a very rare inborn error of immunity, the pathomechanism and clinical spectrum of which overlaps with TAP deficiencies.

10.1016/j.jaci.2024.06.003

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JAK inhibitors to treat STAT3 gain-of-function: a single-center report and literature review

Frontiers in Immunology (2024)

Faranaz Atschekzei Stephan Traidl Julia Carlens Katharina Schütz Sandra von Hardenberg

The signal transducer and activator of transcription 3 (STAT3) gain-of-function (GOF) syndrome (STAT3-GOF) is an inborn error of immunity (IEI) characterized by diverse manifestations of immune dysregulation that necessitate systemic immunomodulatory treatment. The blockade of the interleukin-6 receptor and/or the inhibition of the Janus kinases has been commonly employed to treat diverse STAT3-GOF-associated manifestations. However, evidence on long-term treatment outcome, especially in the case of adult patients, is scarce.

Immune Dysregulation

10.3389/fimmu.2024.1400348

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Novel hypermorphic variants in IRF2BP2 identified in patients with common variable immunodeficiency and autoimmunity

Clinical Immunology (2024)

Manfred Anim Georgios Sogkas Nadezhda Camacho-Ordóñez Gunnar Schmidt Abdulwahab Elsayed

Jurkat cells

Common Variable Immunodeficiency

Wild type

10.1016/j.clim.2024.110326

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Polyphenolic Compounds in Canned Apricots

Journal of Food Science (1965)

Abdulwahab Elsayed B. S. Luh

SUMMARY Polyphenolic compounds were extracted with ethyl acetate from aqueous infusions of canned Blenheim apricots ( Prunus armenica L.). The compounds were separated by two‐dimensional paper chromatography of the extract with n ‐butanol‐acetic acid‐water (4:1:5) and 2% acetic acid. The individual compounds were identified by R f values, fluorescent behavior, absorption spectra, and degradation products. Shown to be present in the extract were three chlorogenic acid isomers, two p ‐coumaric acid derivatives, rutin, isoquercitrin, quercetin, an unidentified quercetin glucoside, catechin, and epicatechin. The predominant polyphenolic compounds were chlorogenic acids and p ‐coumaric acid derivatives.

Chlorogenic Acid

p-Coumaric acid

10.1111/j.1365-2621.1965.tb01879.x

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ChemInform Abstract: Ethyl Chloroformate/DMF in Organic Synthesis. Part 1. A Novel Reagent for Ring Closure of 5‐Amino‐1‐aryl‐4‐imidazolecarboxamides to Their Hypoxanthine Derivatives.

ChemInform (1989)

Khairy A. M. El‐Bayouki Abdulwahab Elsayed Wahid M. Basyouni

Abstract The reaction between the 5‐amino‐4‐imidazolecarboxamides (I) and a mixture of DMF (II) and ethyl chloroformate proceeds under comparatively mild conditions to afford the hypoxanthine derivatives (III) instead of the expected xanthines.

Ethyl chloroformate

Hypoxanthine

Chloroformate

Closure (psychology)

10.1002/chin.198933200

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Rituximab to treat prolidase deficiency due to a novel pathogenic copy number variation inPEPD

RMD Open (2023)

Faranaz Atschekzei Mykola Fedchenko Abdulwahab Elsayed Natalia Dubrowinskaja Theresa Graalmann

Prolidase deficiency (PD) is a rare autosomal recessive inborn error of immunity caused by biallelic homozygous or compound heterozygous loss-of-function mutations in PEPD, the gene that encodes prolidase. PD typically manifests with variable dysmorphic features, chronic cutaneous ulcers, recurrent infections and autoimmune features, including systemic lupus erythematosus. So far, there is no consensus regarding treatment of PD and its autoimmune manifestations. Here, we present a 28-year-old female patient with PD due to a novel homozygous intragenic deletion in PEPD, diagnosed at the age of 6 years and 7 months with an undifferentiated connective tissue disease that, apart from its very early onset, would be consistent with the diagnosis of Sjögren's syndrome. Steroids and diverse conventional synthetic disease-modifying antirheumatic drugs failed to control PD-associated vasculitis and mucocutaneous ulcerations and led to infectious complications, including cytomegalovirus colitis. Introduction of rituximab (RTX) treatment in this patient led to sustained recession of mucocutaneous ulceration, enabling tapering of steroids. High interleukin-1β (IL-1β) production by this patient's monocytes, together with the detection of both IL-1β and interleukin-18 (IL-18) in her serum, suggest enhanced inflammasome activation in PD, whereas the therapeutic efficacy of RTX implies a role for CD20 positive B cells in the complex immunopathogenesis of PD.

Chronic mucocutaneous candidiasis

Mucocutaneous zone

Chronic Granulomatous Disease

Compound heterozygosity

10.1136/rmdopen-2023-003507

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Citations (4)