title: Thymocyte depletion affects neurotrophin receptor expression in thymic stromal cells.
abstract: Thymocytes and thymic stromal cells cross-talk in a bidirectional manner within the thymus, thus contributing to the generation of mature T-cells. The thymic stromal cells in the rat express the high- (TrkA, TrkB) and low-affinity (p75NTR) receptors for neurotrophins. In this study we analysed the regulation of TrkA, TrkB and p75NTR expression in the rat thymus by thymocytes. We induced thymocyte apoptosis by administration of corticoids in rats, and then analysed the expression and distribution of these receptors 1, 4 and 10 days later. Thymocyte death was assessed by the activation of caspase-3 in cells undergoing apoptosis. We observed massive thymocyte apoptosis 1 day after injection and, to a lesser extent, after 4 days, which was parallel with a reduction in the density of thymic epithelial cells normally expressing TrkA and p75NTR. Furthermore, TrkA expression was found in cortical thymic epithelial cells, which normally lack this receptor. The expression of TrkB was restricted to a subset of macrophage-dendritic cells, and remained unchanged with treatment. The normal pattern of neurotrophin receptor expression was almost completely restored by day 10. The results demonstrate that the expression of neurotrophin receptors by thymic epithelial cells, but not by macrophage-dendritic cells, is regulated by thymocytes.
authors.affiliation: Departamento de Morfología y Biología Celular, Universidad de Oviedo, Spain.
authors.forename: P
authors.initials: P
authors.lastname: Pérez-Piñera
authors.forename: O
authors.initials: O
authors.lastname: García-Suarez
authors.forename: J G
authors.initials: JG
authors.lastname: Prieto
authors.forename: A
authors.initials: A
authors.lastname: Germana
authors.forename: E
authors.initials: E
authors.lastname: Ciriaco
authors.forename: M E
authors.initials: ME
authors.lastname: del Valle
authors.forename: J A
authors.initials: JA
authors.lastname: Vega
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3; D020169:Caspases / Q000032:analysis; D003907:Dexamethasone / Q000494:pharmacology; D015536:Down-Regulation; D004847:Epithelial Cells / Q000737:chemistry / Q000378:metabolism; D005938:Glucocorticoids / Q000494:pharmacology; D007150:Immunohistochemistry / Q000379:methods; D018655:Lymphocyte Count; D008212:Lymphocyte Depletion; D008214:Lymphocytes / Q000187:drug effects / Q000378:metabolism*; D008264:Macrophages / Q000737:chemistry; D008297:Male; D009414:Nerve Growth Factors / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020800:Receptor, Nerve Growth Factor / Q000032:analysis / Q000378:metabolism; D020917:Receptor, trkA / Q000032:analysis / Q000378:metabolism; D020813:Receptor, trkB / Q000032:analysis / Q000378:metabolism; D017475:Receptors, Nerve Growth Factor / Q000032:analysis / Q000378:metabolism*; D017154:Stromal Cells / Q000187:drug effects / Q000378:metabolism*; D013950:Thymus Gland / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors
chemical_list: D005938:Glucocorticoids; D009414:Nerve Growth Factors; D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D003907:Dexamethasone; D020917:Receptor, trkA; D020813:Receptor, trkB; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases