| First Author | So AY | Year | 2012 |
| Journal | Blood | Volume | 120 |
| Issue | 12 | Pages | 2428-37 |
| PubMed ID | 22791292 | Mgi Jnum | J:189161 |
| Mgi Id | MGI:5444559 | Doi | 10.1182/blood-2012-04-426247 |
| Citation | So AY, et al. (2012) Regulation of APC development, immune response, and autoimmunity by Bach1/HO-1 pathway in mice. Blood 120(12):2428-37 |
| abstractText | APCs are essential for innate and adaptive immunity as well as self-immune tolerance. Here, we show that the Cap'n'collar member Bach1 regulates the generation of APCs, specifically macrophages and dendritic cells, in mice. The impaired APC development in Bach1(-/-) mice was accompanied by defects in downstream T-cell responses and partial protection from experimental autoimmune encephalomyelitis. Genomewide analyses identified a panel of Bach1 target genes and ablation of the direct Bach1 target gene HO-1 exacerbated the impaired APC development observed in Bach1(-/-) mice. This was attributed to the impaired ability of HO-1(-/-)Bach1(-/-) double mutants to produce upstream APC progenitor cells, including common myeloid progenitor (CMP)-Flk2(+). By contrast, we observed an increase in hematopoietic stem-progenitor cells (HSPCs) in these mice, suggesting a developmental block in the progression of HSPCs to CMP-Flk2(+) and subsequently APCs. |
