| First Author | Gabrilovich DI | Year | 2002 |
| Journal | J Leukoc Biol | Volume | 72 |
| Issue | 2 | Pages | 285-96 |
| PubMed ID | 12149419 | Mgi Jnum | J:78137 |
| Mgi Id | MGI:2183611 | Citation | Gabrilovich DI, et al. (2002) H1(0) histone and differentiation of dendritic cells. A molecular target for tumor-derived factors. J Leukoc Biol 72(2):285-96 |
| abstractText | Dendritic cells (DC) play a central role in antitumor immune responses. Abnormal differentiation of DC and their inability to stimulate T cells are important factors in tumor escape from immune-system control. However, the mechanisms of this process remain elusive. Here, we have described one possible molecular mechanism that involves replacement linker histone H1 (0). A close association between expression of H1(0) and DC differentiation in vitro has been found. DC production in H1(0) -deficient mice was decreased significantly, whereas generation and function of macrophages, granulocytes, and lymphocytes appear to be normal. However, these mice had a significantly reduced response to vaccination with antigens. Tumor-derived factors considerably reduced H1(0) expression in hematopoietic progenitor cells. We have demonstrated that transcription factor NF-kappaB is involved actively in regulation of H1(0). Thus, H1(0) histone may be an important factor in normal DC differentiation. Tumor-derived factors may inhibit DC differentiation by affecting H1(0) expression. |
