| First Author | Kersh EN | Year | 2006 |
| Journal | J Immunol | Volume | 177 |
| Issue | 6 | Pages | 3821-6 |
| PubMed ID | 16951344 | Mgi Jnum | J:138049 |
| Mgi Id | MGI:3804116 | Doi | 10.4049/jimmunol.177.6.3821 |
| Citation | Kersh EN (2006) Impaired memory CD8 T cell development in the absence of methyl-CpG-binding domain protein 2. J Immunol 177(6):3821-6 |
| abstractText | Intracellular differentiation events that determine which cells develop into memory CD8 T cells are currently incompletely understood. Methyl-CpG-binding domain protein 2 (MBD2) is a transcriptional repressor that binds to methylated DNA and mediates the biological consequences of epigenetic gene methylation. The role of MBD2 during the differentiation of naive CD8 T cells into effector and memory cells was determined following acute infection of MBD2-deficient mice with lymphocytic choriomeningitis virus. Despite rapid viral clearance and an efficient primary effector CD8 T cell response, reduced numbers of Ag-specific memory CD8 T cells were observed. Importantly, the appearance of precursor memory cells (IL-7Ralphahigh) was delayed. The remaining MBD2(-/-) memory cells were not fully protective during rechallenge, and memory cell characteristics were altered with regard to surface markers (IL-7Ralpha, KLRG-1, CD27, and others) and cytokine production. The defect was CD8 T cell intrinsic, because memory cell development was also delayed when MBD2(-/-) CD8 T cells were adoptively transferred into SCID mice. These data demonstrate that MBD2 is a previously unrecognized intracellular factor required for the efficient generation of protective memory CD8 T cells. |
