Restraint of B Cell Activation by Foxj1-Mediated Antagonism of NF-κB and IL-6
Copyright policy )Restraint of B Cell Activation by Foxj1-Mediated Antagonism of NF-κB and IL-6
AbstractThe 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.
- University of Mary United States
- Washington University in St. Louis United States
Mice, Knockout, B-Lymphocytes, Mice, Inbred BALB C, Mice, Inbred MRL lpr, Base Sequence, Mice, Inbred NZB, Interleukin-6, Molecular Sequence Data, NF-kappa B, Mice, Nude, Forkhead Transcription Factors, Lymphocyte Activation, DNA-Binding Proteins, Mice, Inbred C57BL, Mice, Antibody Formation, Animals, Binding Sites, Antibody, Cells, Cultured, Autoantibodies
Mice, Knockout, B-Lymphocytes, Mice, Inbred BALB C, Mice, Inbred MRL lpr, Base Sequence, Mice, Inbred NZB, Interleukin-6, Molecular Sequence Data, NF-kappa B, Mice, Nude, Forkhead Transcription Factors, Lymphocyte Activation, DNA-Binding Proteins, Mice, Inbred C57BL, Mice, Antibody Formation, Animals, Binding Sites, Antibody, Cells, Cultured, Autoantibodies
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