| First Author | Majumder P | Year | 2014 |
| Journal | J Immunol | Volume | 192 |
| Issue | 8 | Pages | 3925-35 |
| PubMed ID | 24634495 | Mgi Jnum | J:210008 |
| Mgi Id | MGI:5569227 | Doi | 10.4049/jimmunol.1303205 |
| Citation | Majumder P, et al. (2014) B cell differentiation is associated with reprogramming the CCCTC binding factor-dependent chromatin architecture of the murine MHC class II locus. J Immunol 192(8):3925-35 |
| abstractText | The transcriptional insulator CCCTC binding factor (CTCF) was shown previously to be critical for human MHC class II (MHC-II) gene expression. Whether the mechanisms used by CTCF in humans were similar to that of the mouse and whether the three-dimensional chromatin architecture created was specific to B cells were not defined. Genome-wide CTCF occupancy was defined for murine B cells and LPS-derived plasmablasts by chromatin immunoprecipitation sequencing. Fifteen CTCF sites within the murine MHC-II locus were associated with high CTCF binding in B cells. Only one-third of these sites displayed significant CTCF occupancy in plasmablasts. CTCF was required for maximal MHC-II gene expression in mouse B cells. In B cells, a subset of the CTCF regions interacted with each other, creating a three-dimensional architecture for the locus. Additional interactions occurred between MHC-II promoters and the CTCF sites. In contrast, a novel configuration occurred in plasma cells, which do not express MHC-II genes. Ectopic CIITA expression in plasma cells to induce MHC-II expression resulted in high levels of MHC-II proteins, but did not alter the plasma cell architecture completely. These data suggest that reorganizing the three-dimensional chromatin architecture is an epigenetic mechanism that accompanies the silencing of MHC-II genes as part of the cell fate commitment of plasma cells. |
