| First Author | Dhaeze T | Year | 2019 |
| Journal | Cell Mol Immunol | Volume | 16 |
| Issue | 7 | Pages | 652-665 |
| PubMed ID | 30635649 | Mgi Jnum | J:298779 |
| Mgi Id | MGI:6488687 | Doi | 10.1038/s41423-018-0198-5 |
| Citation | Dhaeze T, et al. (2019) CD70 defines a subset of proinflammatory and CNS-pathogenic TH1/TH17 lymphocytes and is overexpressed in multiple sclerosis. Cell Mol Immunol 16(7):652-665 |
| abstractText | CD70 is the unique ligand of CD27 and is expressed on immune cells only upon activation. Therefore, engagement of the costimulatory CD27/CD70 pathway is solely dependent on upregulation of CD70. However, the T cell-intrinsic effect and function of human CD70 remain underexplored. Herein, we describe that CD70 expression distinguishes proinflammatory CD4(+) T lymphocytes that display an increased potential to migrate into the central nervous system (CNS). Upregulation of CD70 on CD4(+) T lymphocytes is induced by TGF-beta1 and TGF-beta3, which promote a pathogenic phenotype. In addition, CD70 is associated with a TH1 and TH17 profile of lymphocytes and is important for T-bet and IFN-gamma expression by both T helper subtypes. Moreover, adoptive transfer of CD70(-/-)CD4(+) T lymphocytes induced less severe experimental autoimmune encephalomyelitis (EAE) disease than transfer of WT CD4(+) T lymphocytes. CD70(+)CD4(+) T lymphocytes are found in the CNS during acute autoimmune inflammation in humans and mice, highlighting CD70 as both an immune marker and an important costimulator of highly pathogenic proinflammatory TH1/TH17 lymphocytes infiltrating the CNS. |
