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Antigen‐induced Lymph Node Remodeling: LVs, HEVs and Conduits
Author(s) -
Stranford Sharon A,
Liao Shan,
Bentley Kevin,
Ruddle Frank H.,
Ruddle Nancy H
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.392.3
Subject(s) - lymphatic system , high endothelial venules , lymph , antigen , lymph node , microbiology and biotechnology , chemistry , green fluorescent protein , lymphatic vessel , lymphatic endothelium , transgene , immune system , immunology , pathology , biology , gene , medicine , biochemistry , genetics , cancer , metastasis
Secondary lymphoid organs are the sites of antigen encounter with naïve, antigen‐specific lymphocytes, and as such are crucial to the development of acquired immunity. In lymph nodes (LNs), this process is facilitated by the convergence of high endothelial venules (HEVs) and lymphatic vessels (LVs) delivering lymphocytes and tissue‐derived antigen, respectively. Conduits, a third system of channels, may directly connect the afferent lymphatics with the abluminal surface of HEVs, facilitating rapid communication between the two. We investigated the relationship of these structures in draining LNs during antigen encounter. Mice transgenic for HEC‐6ST (an HEV unique gene) driving eGFP expression were skin painted with oxazalone. Four days later, draining LNs were removed and sections were stained for LV‐, HEV‐ and conduit‐specific markers. At day 4, expression of HEC‐6ST was suppressed, with concomitant enhancement of MAd‐CAM‐1 expression, a marker of an immature HEV phenotype. Surprisingly, the endothelial cells of some vessels expressed both Lyve‐1 and PNAd, or displayed a mixture of HEC‐6ST+ and Lyve‐1+ cells. The ER‐TR7+ conduit network permeated the T cell areas and surrounded HEVs. These data demonstrate that Hec6st‐egfp transgenic mice can be used to evaluate vascular interactions in draining LNs. Supported by NIH CA16885 and DK50731 (NHR) and NIH R15 AI051674‐02 (SAS).