Glucocorticoid inhibition of activation-induced cytidine deaminase expression in human B lymphocytes

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

We examined whether glucocorticoids could modulate the expression of activation-induced cytidine deaminase (AICDA), the principal regulator of the processes of immunoglobulin gene somatic hypermutation and class switch recombination in B lymphocytes. Treatment of human B cells with IL-4 and anti-CD40 antibody for 18-20. h resulted in induction of expression of AICDA mRNA by over 10-fold. Dexamethasone at 10. nM concentration inhibited AICDA induction by an average of 51.8% (p< 0.0001). These effects of glucocorticoids were found to be dose dependent in the physiologic range and were reversible by co-treatment with a glucocorticoid receptor antagonist. Human B cell viability and proliferation were unaltered by glucocorticoid treatment. These data demonstrate that physiologic concentrations of glucocorticoids can act on human B lymphocytes through glucocorticoid receptor-mediated mechanisms to diminish the expression of AICDA, a key regulator of humoral immune responses.

Original languageEnglish (US)
Pages (from-to)881-887
Number of pages7
JournalMolecular and Cellular Endocrinology
Volume382
Issue number2
DOIs
Publication statusPublished - Feb 15 2014

    Fingerprint

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Cite this