| First Author | Onder L | Year | 2013 |
| Journal | J Exp Med | Volume | 210 |
| Issue | 3 | Pages | 465-73 |
| PubMed ID | 23420877 | Mgi Jnum | J:196703 |
| Mgi Id | MGI:5489042 | Doi | 10.1084/jem.20121462 |
| Citation | Onder L, et al. (2013) Endothelial cell-specific lymphotoxin-beta receptor signaling is critical for lymph node and high endothelial venule formation. J Exp Med 210(3):465-73 |
| abstractText | The development of lymph nodes (LNs) and formation of LN stromal cell microenvironments is dependent on lymphotoxin-beta receptor (LTbetaR) signaling. In particular, the LTbetaR-dependent crosstalk between mesenchymal lymphoid tissue organizer and hematopoietic lymphoid tissue inducer cells has been regarded as critical for these processes. Here, we assessed whether endothelial cell (EC)-restricted LTbetaR signaling impacts on LN development and the vascular LN microenvironment. Using EC-specific ablation of LTbetaR in mice, we found that conditionally LTbetaR-deficient animals failed to develop a significant proportion of their peripheral LNs. However, remnant LNs showed impaired formation of high endothelial venules (HEVs). Venules had lost their cuboidal shape, showed reduced segment length and branching points, and reduced adhesion molecule and constitutive chemokine expression. Due to the altered EC-lymphocyte interaction, homing of lymphocytes to peripheral LNs was significantly impaired. Thus, this study identifies ECs as an important LTbetaR-dependent lymphoid tissue organizer cell population and indicates that continuous triggering of the LTbetaR on LN ECs is critical for lymphocyte homeostasis. |
