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Updated: Jun 22, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
10:27

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Published on: December 15, 2011

[IgA subclass and IgA deficiency].

Hideo Kaneko1, Hiroko Suzuki, Naomi Kondo

  • 1Division of Pediatrics, Center for Regional Medicine, Gifu University, Gifu, Japan.

Nihon Rinsho Men'Eki Gakkai Kaishi = Japanese Journal of Clinical Immunology
|July 1, 2009
PubMed
Summary
This summary is machine-generated.

The alpha1 gene deletion is identified as a cause of selective Immunoglobulin A (IgA) deficiency (IgAD), a common immunodeficiency. This finding helps understand partial IgAD pathogenesis.

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14:18

Dioscin Mediated IgA Nephropathy Alleviation by Inhibiting B Cell Activation In Vivo and Decreasing Galactose-Deficient IgA1 Production In Vitro

Published on: October 13, 2023

Area of Science:

  • Immunology
  • Genetics

Context:

  • Immunoglobulin A (IgA) comprises two subclasses, IgA1 and IgA2, encoded by distinct alpha1 and alpha2 genes.
  • These subclasses are crucial for mucosal immunity, with varying ratios in secretions.
  • Selective IgA deficiency (IgAD), the most common immunodeficiency, often has an unknown cause, though B cell class switch disorders are implicated.

Purpose:

  • To investigate the genetic basis of selective IgA deficiency (IgAD).
  • To evaluate the role of alpha1 and alpha2 gene expression in IgAD pathogenesis.
  • To identify genetic causes for partial IgAD.

Summary:

  • The study identified the second case of alpha1 gene deletion in Japan using RT-PCR to analyze alpha1 and alpha2 mRNA levels.
  • Low expression of alpha1 and alpha2 genes is observed in most IgAD patients.
  • Patients with alpha1 gene deletion exhibit partial IgAD, characterized by specific IgA subclass deficiency.

Impact:

  • This research clarifies a genetic cause for partial IgA deficiency.
  • It provides a basis for diagnosing and understanding IgAD.
  • Contributes to the understanding of B cell class switch mechanisms in IgAD.