Control of Inflammation, Cytokine Expression, and Germinal Center Formation by BCL-6

Abstract

The gene encoding the BCL-6 transcriptional repressor is frequently translocated and mutated in diffuse large cell lymphoma. Mice with a disrupted BCL-6 gene developed myocarditis and pulmonary vasculitis, had no germinal centers, and had increased expression of T helper cell type 2 cytokines. The BCL-6 DNA recognition motif resembled sites bound by the STAT (signal transducers and activators of transcription) transcription factors, which mediate cytokine signaling. BCL-6 could repress interleukin-4 (IL-4)–induced transcription when bound to a site recognized by the IL-4–responsive transcription factor Stat6. Thus, dysregulation of STAT-responsive genes may underlie the inflammatory disease in BCL-6–deficient mice and participate in lymphoid malignancies.

Keywords

Germinal centerTranscription factorBiologySTAT6CytokinestatSTAT4RepressorCancer researchTranscription (linguistics)STAT3Cell biologyGeneSignal transductionImmunologyB cellGeneticsAntibody

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Publication Info

Year: 1997
Type: article
Volume: 276
Issue: 5312
Pages: 589-592
Citations: 919
Access: Closed

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APA Style

                            
                                
                                    Alexander L. Dent, 
                                
                                    Arthur L. Shaffer, 
                                
                                    Xin Yu
                                
                                et al.
                            
                            (1997). 
                            Control of Inflammation, Cytokine Expression, and Germinal Center Formation by BCL-6. 
                            Science
                            , 276
                            (5312)
                            , 589-592.
                            https://doi.org/10.1126/science.276.5312.589
                        

Identifiers

DOI: 10.1126/science.276.5312.589