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The Journal of Immunology, 1998, 161: 1837-1843.
Copyright © 1998 by The American Association of Immunologists

Translational Control of MHC Class II I-A Molecules by IFN-{gamma}1

Eduard Goñalons*, Marta Barrachina*, José A. García-Sanz{dagger} and Antonio Celada2,*

* Departament de Fisiologia (Immunologia), Facultat de Biologia and Fundacio August Pi i Sunyer, Campus de Bellvitge, Universitat de Barcelona, Barcelona, Spain; and {dagger} Basel Institute for Immunology, Basel, Switzerland and Department of Immunology and Oncology, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones Cientificas, Madrid, Spain

MHC class II molecules are expressed in a limited number of cell types, including B lymphocytes and macrophages (M{phi}). IFN-{gamma} increases the surface expression of class II molecules in a murine B cell line without inducing detectable changes in either I-A or I-A mRNA levels. In bone marrow-derived M{phi}, IFN-{gamma} causes an increase in class II expression at both the mRNA and surface levels. In addition to the increase in transcription rates described for M{phi}, IFN-{gamma} increases the rate of synthesis of IA{alpha} and IAß proteins and the ribosome loading for both mRNA molecules in both cell types. Interestingly, there is a significant peak of free I-A mRNA in noninduced cells. Therefore, IFN-{gamma} regulates the expression of MHC class II molecules at the translational level in both B cells and M{phi} and, as already reported, at the transcriptional level only in M{phi}. The actual mechanism of regulation causes changes in the translation initiation rates in both cell types, as demonstrated by an increase in ribosome loading in polysome gradients.




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