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Thymic epithelial cells of human patients affected by myasthenia gravis overexpress IGF-I immunoreactivity

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Abstract:

Marinova TT, Kuerten S, Petrov DB, Angelov DN. Thymic epithelial cells of human patients affected by myasthenia gravis overexpress IGF-I immunoreactivity. APMIS 2008;116:50–58.

Accumulating evidence shows that several kinds of thymic cells express insulin-like growth factor-I (IGF-I), which is known to play an important role in T cell ontogeny under both physiological and pathological conditions. Still, little is known about the mechanisms of IGF-I involvement in the pathological transformation of the thymocyte microenvironment. The present study focuses on a comparative analysis of the IGF-I immunoreactivity of thymic epithelial cells (EC) from human patients with hyperplasia-associated myasthenia gravis (MG) versus physiological thymic tissue from healthy controls using immunohistochemistry and immunoelectron microscopy. We show that myasthenic EC overexpress IGF-I in comparison to EC from control subjects. The IGF-I immunoreactivity in the medullary and cortical EC from MG patients was stronger than in the normal gland. The increased expression of IGF-I and more frequent distribution of IGF-I and IGF-I-receptor (IGF-IR) immunopositive EC correlated with modulation in the immunoreactivity of double (IGF-I/IGF-IR) positive EC. Our data provide new immunocytochemial evidence for alterations of IGF-I and IGF-IR immunoreactivity in EC from pathological thymi. The persisting expression of IGF-I and IGF-IR most likely indicates that the myasthenic thymus is still capable of governing IGF-I signaling pathways, which are involved in the local regulation of T cell development and plasticity.

Keywords: IGF-I; IGF-IR; human thymus; immunoreactivity; myasthenia gravis; thymic epithelial cells

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1600-0463.2008.00666.x

Affiliations: 1: Surgery, Medical University Sofia, Bulgaria 2: Department of Anatomy I, University of Cologne, Germany

Publication date: January 1, 2008

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