Immunohistochemical Study of TrkA Neurotrophin Receptor Expression during Thymic Regeneration / 대한해부학회지

ABSTRACT

Numerous studies have demonstrated interactions between the nervous/endocrine and the immune system. Increasing evidence suggests that some members of neurotrophins such as nerve growth factor (NGF) are involved in the control of immune system. Recent studies have demonstrated that the TrkA receptor, which serves as the high affinity receptor for NGF and neurotrophin-3 (NT-3), is expressed in thymic epithelial cells. In the present study, we investigated the expression of the TrkA receptor in the rat thymus from a model of thymic involution and regeneration induced by cyclophosphamide. After single dose of cyclophosphamide (150 mg/kg) was administered to Sprague-Dawley rats by intraperitoneal injection, the rats were sacrificed at 3, 7 and 14 days. The immunocytochemical characterization of the thymus was carried out using cryostat-cut sections. We found an increased expression of TrkA immunoreactivity in the thymic epithelial cells, especially in the subcapsular epithelial cells in cyclophosphamide-treated rats. The cortical epithelial cells also showed an increased expression of TrkA immunoreactivity after cyclophosphamide treatment, although the expression level was lower than that of the thymic subcapsular epithelial cells. However, there was no significant alteration of TrkA immunoreactivity in the medullary epithelial cells of the thymus from cyclophosphamide-treated rats. In general, most of these phenomena disappeared two weeks after cyclophosphamide administration and thus, the immunohistochemical features became to be similar to those of normal thymus. In conclusion, it may be speculated that TrkA receptor via interaction with their ligands provides an important signal to the thymic epithelial cells, especially to the subcapsular epithelial cells, for the thymic regeneration during recovery from acute thymic involution. Thus, our results support the proposed immunoregulatory role of neurotrophins.