한빛사 논문
Abstract
Raghu P. Kataru,1,2,6 Honsoul Kim,1,2,6 Cholsoon Jang,1,3 Dong Kyu Choi,1,3 Bong Ihn Koh,1,2 Minah Kim,1,3 Sudheer Gollamudi,1,3 Yun-Keun Kim,5 Seung-Hyo Lee,2,* and Gou Young Koh1,2,3,4,*
1National Research Laboratory of Vascular Biology
2Graduate School of Medical Science and Engineering
3Department of Biological Sciences
4Graduate School of Nanoscience & Technology (WCU)
Korea Advanced Institute of Science and Technology (KAIST), Daejeon, 305-701, Korea
5Department of Life Science and Division of Molecular and Life Sciences, Pohang University of Science and Technology, Pohang, 790-784, Korea
6These authors contributed equally to this work
*Correspondence: S.-H.L., G.Y.K.
SUMMARY
Lymph node lymphatic vessels (LNLVs) serve as a conduit to drain antigens from peripheral tissues to within the lymph nodes. LNLV density is known to be positively regulated by vascular endothelial growth factors secreted by B cells, macrophages, and dendritic cells (DCs). Here, we show that LNLV formation was negatively regulated by T cells. In both steady and inflammatory states, the density of LNLVs was increased in the absence of T cells but decreased when T cells were restored. Interferon-g secretion by T cells suppressed lymphatic-specific genes in lymphatic endothelial cells and consequently caused marked reduction in LNLV formation. When T cells were depleted, recruitment of antigencarrying DCs to LNs was augmented, reflecting a compensatory mechanismfor antigen presentation to T cells through increased LNLVs. Thus, T cells maintain the homeostatic balance of LNLV density through a negative paracrine action of interferon-g.
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