Restraint of B cell activation by Foxj1-mediated antagonism of NF-κB and IL-6

Ling Lin, Steven L. Brody, Stanford L. Peng

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

The forkhead transcription factor Foxj1 inhibits spontaneous autoimmunity, in part by antagonizing NF-κB activation in T cells. We demonstrate here that Foxj1 also inhibits humoral immune responses intrinsically in B cells; Foxj1 deficiency in B cells results in spontaneous and accentuated germinal center formation, associated with the development of pathogenic autoantibodies and accentuated responses to immunizations-all reflecting excessive activity of NF-κB and its target gene IL-6, and correlating with a requirement for Foxj1 to regulate the inhibitory NF-κB. component IκBβ. Thus, Foxj1 restrains B cell activation and the maturation of humoral responses, demonstrating a critical role for at least this forkhead transcription factor in the regulation of B lymphocyte homeostasis.

Original languageEnglish
Pages (from-to)951-958
Number of pages8
JournalJournal of Immunology
Volume175
Issue number2
StatePublished - Jul 15 2005

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