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Restraint of B Cell Activation by Foxj1-Mediated Antagonism of NF-B and IL-6¹

Ling Lin^*, Steven L. Brody and Stanford L. Peng^2,*,

^* Division of Rheumatology and Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine and Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110

The forkhead transcription factor Foxj1 inhibits spontaneous autoimmunity, in part by antagonizing NF-B 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-B and its target gene IL-6, and correlating with a requirement for Foxj1 to regulate the inhibitory NF-B component IB. 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.

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