UEA-I-binding to thymic medullary epithelial cells selectively reduces numbers of cortical TCRαβ+ thymocytes in FTOCs

Thymic medullary epithelial cells (TMECs) constitute a major stromal cell type, the function of which is incompletely understood. Some TMECs express L-fucose-glycosylated proteins on their plasma membrane; these have been shown to specifically bind the lectin UEA-I. We exploited this observation to investigate the consequences of in situ blockage of TMECs in FTOCs by UEA-I. In UEA-I-treated FTOCs, we noted a decreased cellularity among TCR alpha beta (+) but not TCR gamma delta (+) cells. In fact, CD3(-) and CD3(1 omicron) cortical cells were markedly depleted, while CD3(h1) cells were unaffected. Since the affected cell subsets are in a different compartment from that where UEA-I binding occurs, it is likely that the effect is mediated through a soluble factor. Two possible mechanisms are proposed: a reduced activation of either TMECs or of medullary thymocytes which normally bind to them, results in lowered production of soluble factors responsible for cortical thymocyte proliferation. Alternately, the binding of UEA-I to TMECs could activate the latter to produce signals inhibitory to cortical thymocytes. (C) 2001 Elsevier Science B.V. All rights reserved.