Schwann cell differentiation inhibits interferon-gamma induction of expression of major histocompatibility complex class ii and intercellular adhesion molecule-1

• Published in: Journal of neuroimmunology 2016-06, Vol.295-296, p.93-99
• Main Authors: Lisak, Robert P, Bealmear, Beverly, Benjamins, Joyce A
• Format: Article
• Language: English
• Subjects: 8-Bromo Cyclic Adenosine Monophosphate - pharmacology; Allergy and Immunology; Animals; Animals, Newborn; Axolemma; Cell Differentiation - drug effects; Cells, Cultured; Cytokines; Demyelinating neuropathy; Dose-Response Relationship, Drug; Drug Interactions; Gene Expression Regulation - drug effects; Histocompatibility Antigens Class II - metabolism; Intercellular Adhesion Molecule-1 - metabolism; Interferon; Interferon-gamma - pharmacology; Neurology; Peripheral nervous system; Rats; Schwann cells; Schwann Cells - drug effects; Time Factors
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/j.jneuroim.2016.03.013

Abstract Interferon-gamma (IFN-γ) upregulates major histocompatibility complex class II (MHC class II) antigens and intercellular adhesion molecule-1 (ICAM-1) on Schwann cells (SC) in vitro , but in nerves of animals and patients MHC class II is primarily expressed on inflammatory cells. We investigated whether SC maturation influences their expression. IFN-γ induced MHC class II and upregulated ICAM-1; the axolemma-like signal 8-bromo cyclic adenosine monophosphate (8 Br cAMP) with IFN-γ inhibited expression. Delaying addition of 8 Br cAMP to SC already exposed to IFN-γ inhibited ongoing expression; addition of IFN-γ to SC already exposed to 8 Br cAMP resulted in minimal expression. Variability of cytokine-induced MHC class II and ICAM-1 expression by SC in vivo may represent the variability of signals from axolemma.