Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 2, Pages 951-958Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.2.951
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- NIAID NIH HHS [AI 057471, AI 061478] Funding Source: Medline
- NIDDK NIH HHS [DK 52574] Funding Source: Medline
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The forkhead transcription factor Foxj1 inhibits spontaneous autoimmunity, in part by antagonizing NF-kappa 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-kappa B and its target gene IL-6, and correlating with a requirement for Foxj1 to regulate the inhibitory NF-kappa B component I kappa B beta. 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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