Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 45, Issue 8, Pages 2212-2217Publisher
WILEY-BLACKWELL
DOI: 10.1002/eji.201545634
Keywords
Killer cell lectin-like receptor G1; alpha(E) (CD103); E-cadherin; CD8(+) T cell; TGF-beta
Categories
Funding
- Deutsche Forschungsgemeinschaft DFG [PI 295/7-1]
- European Union (EFRE, INTERREG IV Oberrhein) [A30]
Ask authors/readers for more resources
The inhibitory receptor killer cell lectin-like receptor G1 (KLRG1) and the integrin alpha(E) (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 aremutually 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available