Female agammaglobulinemia due to the Bruton tyrosine kinase deficiency caused by extremely skewed X-chromosome inactivation

Blood. 2004 Jan 1;103(1):185-7. doi: 10.1182/blood-2003-06-1964. Epub 2003 Sep 4.

Abstract

We analyzed the cause of agammaglobulinemia in a girl whose father had been diagnosed as having X-linked agammaglobulinemia (XLA). Flow cytometric analysis revealed the lack of peripheral B cells with the block of B-cell differentiation in the stages between pro-B cells and pre-B cells in the bone marrow, and the defect of the Bruton tyrosine kinase (BTK) expression on monocytes. We found a BTK gene mutation in the first single base pair of intron 11 in her father and heterozygous mutation in the patient at the site. Sequence analysis of abnormally smaller-sized polymerase chain reaction (PCR) products of cDNA confirmed splicing abnormalities due to the mutation. Maternally derived X chromosome was exclusively inactivated in peripheral blood and oral mucosal cells. This is the first report of female XLA caused by heterozygous BTK gene abnormality and extreme nonrandom inactivation of X chromosome on which normal BTK gene is located.

Publication types

  • Case Reports

MeSH terms

  • Agammaglobulinaemia Tyrosine Kinase
  • Agammaglobulinemia / enzymology*
  • Agammaglobulinemia / genetics*
  • Agammaglobulinemia / pathology
  • B-Lymphocytes / immunology
  • B-Lymphocytes / pathology
  • Base Sequence
  • Cell Differentiation
  • Chromosomes, Human, X / genetics
  • DNA, Complementary / genetics
  • Dosage Compensation, Genetic*
  • Female
  • Genetic Linkage
  • Heterozygote
  • Humans
  • Infant
  • Male
  • Point Mutation
  • Protein-Tyrosine Kinases / deficiency*
  • Protein-Tyrosine Kinases / genetics*
  • RNA Splicing / genetics

Substances

  • DNA, Complementary
  • Protein-Tyrosine Kinases
  • Agammaglobulinaemia Tyrosine Kinase
  • BTK protein, human