| First Author | Schwartzkopff S | Year | 2015 |
| Journal | Eur J Immunol | Volume | 45 |
| Issue | 8 | Pages | 2212-7 |
| PubMed ID | 26014037 | Mgi Jnum | J:229119 |
| Mgi Id | MGI:5750827 | Doi | 10.1002/eji.201545634 |
| Citation | Schwartzkopff S, et al. (2015) TGF-beta downregulates KLRG1 expression in mouse and human CD8(+) T cells. Eur J Immunol 45(8):2212-7 |
| abstractText | The inhibitory receptor killer cell lectin-like receptor G1 (KLRG1) and the integrin alphaE (CD103) are expressed by CD8(+) T cells and both are specific for E-cadherin. However, KLRG1 ligation by E-cadherin inhibits effector T-cell function, whereas binding of CD103 to E-cadherin enhances cell-cell interaction and promotes target cell lysis. Here, we demonstrate that KLRG1 and CD103 expression in CD8(+) T cells from untreated and virus-infected mice are mutually exclusive. Inverse correlation of KLRG1 and CD103 expression was also found in human CD8(+) T cells-infiltrating hepatocellular carcinomas. As TGF-beta is known to induce CD103 expression in CD8(+) T cells, we examined whether this cytokine also regulates KLRG1 expression. Indeed, our data further reveal that TGF-beta signaling in mouse as well as in human CD8(+) T cells downregulates KLRG1 expression. This finding provides a rationale for the reciprocal expression of KLRG1 and CD103 in different CD8(+) T-cell subsets. In addition, it points to the limitation of KLRG1 as a marker for terminally differentiated CD8(+) T cells if lymphocytes from tissues expressing high levels of TGF-beta are analyzed. |
