| Abstract: |
The transcriptional repressor protein BCL-6, implicated in the pathogenesis of B cell lymphoma, regulates lymphocyte differentiation and inflammation. We investigated the mechanism for the T helper cell subset 2 (TH2)-type inflammation that occurs in BCL-6-/- mice. Using chimeric mice we found that the TH2-type inflammation is dependent upon nonlymphoid cells. We identified three chemokines, MCP-1, MCP-3 and MRP-1, which are negatively regulated by BCL-6 in macrophages. Promoter analysis revealed that BCL-6 is a potent repressor of MCP-1 transcription. Our results provide a mechanism for the regulation of TH2-type inflammation by BCL-6 and link TH2 differentiation to innate immunity. |
| Keywords: |
dna binding protein; oncoprotein; genetics; dna-binding proteins; proto-oncogene proteins; mouse; animal; cytology; metabolism; mouse mutant; animals; mice; mice, knockout; transcription factor; genetic transcription; transcription, genetic; mice, inbred c57bl; physiology; c57bl mouse; transcription factors; gene expression regulation; germinal center; cytokine; th2 cell; biosynthesis; immunology; cytokines; chemokine; protein bcl 6; monocyte chemotactic protein 3; macrophage; macrophages; monocyte chemotactic protein 1; chemokine ccl2; chemokines; th2 cells; proto-oncogene proteins c-bcl-6; monocyte chemoattractant proteins; chemokines, cc; article; monocyte chemotactic protein; beta chemokine; ccl6 protein, mouse
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