REDUCED LEVELS OF INSULIN-LIKE GROWTH FACTOR-1 RECEPTOR (IGF-1R) SUPPRESS CELLULAR SIGNALING IN EXPERIMENTAL AUTOIMMUNE SIALADENITIS (EAS) W. Mustafa, 1,2, * A. Mustafa, 3 N. Elbakri, 3 H. Link, 2 and A. Adem 3 1 Division of Periodontics, Karolinska Institute, Institute of Odontology, Stockholm, Sweden 2 Division of Neurology and 3 Division of Geriatrics, Neurotec, Huddinge University Hospital, Karolinska Institute, Stockholm, Sweden ABSTRACT The nonobese diabetic mouse (NOD) develops destruction and functional impairment of salivary and lachrymal glands, experimental autoimmune sialadenitis (EAS), resembling and representing a model for Sjo Ègren's syndrome (SS). To investigate the mechanisms of tissue destruction in EAS, we analyzed a cell survival promoter insulin-like growth factor-1 receptor (IGF-1R) in the submandibular glands of NOD mice with this disease. We also evaluated the expression of a downstream effector of IGF-1R, BAD. Receptor- binding autoradiography revealed that the IGF-1R levels in submandibular glands from young NOD mice were lower than those in adult NOD mice. Immuno¯uorescence staining demonstrated that BAD expression in the epithelial cells of the submandibular gland was consistently enhanced through- out the course of EAS in NOD mice. These ®ndings suggest that a reduction in the levels of IGF-1R induces a defective glandular homeostasis in the submandibular gland epithelial cells and triggers EAS. J. OF RECEPTOR & SIGNAL TRANSDUCTION RESEARCH, 21(1), 47±54 (2001) 47 Copyright # 2001 by Marcel Dekker, Inc. www.dekker.com *Corresponding author. Journal of Receptors and Signal Transduction Downloaded from informahealthcare.com by United Arab Emirates University on 11/27/14 For personal use only.