High venule endothelial cells

Each node, also called a lymph gland, has both arterial blood supply and venous drainage. Lymphocytes drain out of the arteries into the node interior, usually through a high endothelial venule that facilitates their entry. This venule (small vein) derives its name from the higher-than-usual tightly joined endothelial cells that line it. 

Figure 1. Interaction between leukocytes and endothelial cells of Mood vessels (modified from [3e]). Top overview bottom single steps with explanation of the symbols. Stimulation of endothelial cells by various mediators and factors leads to the expression of selectins and platelet-activating factor (PAF). The extravasation of leukocytes from the postcapillary venules starts with a weak, low-affinity, selectin-mediated adhesion of the leukocytes to endothelial cells, which leads to a slowing down of the leukocyte velocity (rolling). In the second phase a PAF-mediated activation of the leukocyte integrins occurs. In the third phase the activated integrins bind with high affinity to their ligands which are located on the endothelial cell surface. These ligands are called intercellular cell adhesion molecules (ICAM) and are members of the immunoglobulin superfamily. The firm adhesion of the leukocyte cells to the endothelium and finally their departure from the blood vessel (extravasation) results.

Fig. 197. High endothelial venule (HEV) with a convex adlu-minal surfaces of the endothelial cells in a thoracic lymph node (block 4478) of a 215 g Sprague-Dawley rat (Charles River, France) injected intraperitoneally with 50 mg montmorillonite API H 26 suspended in 2 ml saline. 4 days later under pentobarbital anaesthesia (30 mg/kg), the animal was perfused from the abdominal aorta with 2.5 % glutaraldehyde in 0.1 M sodium cacodylate buffer (pH 7.4). Postfixation with 1 % osmium tetroxide in sodium cacodylate buffer. Embedded in Epon 812 and sectioned at 50 nm. Lead citrate and uranyl acetate. Film 264/79...

Yoneyama H, Matsuno K, Zhang Y, et al. Evidence for recruitment of plasmacytoid dendritic cell precursors to inflamed lymph nodes through high endothelial venules. Int Immunol 2004 16(7) 915-928. 

These processes depend on chemotactic activation of the effector cells and altered cellular migration to promote an allergic reaction. During these events, there is also an upregulation of the adhesion molecules, both on the effector cells and on high endothelial venules in blood vessels, lungs and other tissues. 

Cytokine/chemokine milieu induced by external, self and self-modified proteins, loaded into DCs/macrophages and delivered from affected tissues (including the brain) by lymph into regional draining lymph nodes controls the balance between induction of immunity or tolerance. Both the induction of antigen-specific immunity and tolerance rely on the direct interaction of DCs with naive T cells. These interactions occur in the T cell zone of lymph nodes in the vicinity of high endothelial venules (Von Andrian and Mackay, 2000). 

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