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LPS upregulates MHC class II I-A expression in B lymphocytes at transcriptional and at translational levels
M Barrachina1, E Goñalons, A Celada
1Departament de Fisiologia (Biologia del Macròfag), Facultat de Biologia and Fundació August Pi i sunyer, Universitat de Barcelona, Spain.
Major histocompatibility complex (MHC) class II molecules are expressed in a limited number of cell types, including B lymphocytes, dendritic cells and macrophages. Lipopolysaccharide (LPS) increases the surface expression of class II molecules in a murine B-cell line by inducing an increase in I-A protein and I-A mRNA levels. LPS does not modify the rate of mRNA degradation; therefore, the increase in mRNA is due to an increase in transcription. In addition, LPS increases the levels of I-Aalpha protein, which correlates with an increase in ribosome loading for I-Aalpha but not for I-Abeta mRNA after treatment with LPS. Interestingly, in non-induced cells, I-Aalpha messenger RNA shows a significant peak of free mRNA. Therefore, LPS regulates the expression of MHC class II molecules at translational level in B cells, in addition to the transcriptional control. The actual mechanism implies changes of translation initiation rates, as shown by an increase ribosome loading in polysome gradients.
Major histocompatibility complex (MHC) class II molecules are expressed in a limited number of cell types, including B lymphocytes, dendritic cells and macrophages. Lipopolysaccharide (LPS) increases the surface expression of class II molecules in a murine B-cell line by inducing an increase in I-A protein and I-A mRNA levels. LPS does not modify the rate of mRNA degradation; therefore, the increase in mRNA is due to an increase in transcription. In addition, LPS increases the levels of I-Aalpha protein, which correlates with an increase in ribosome loading for I-Aalpha but not for I-Abeta mRNA after treatment with LPS. Interestingly, in non-induced cells, I-Aalpha messenger RNA shows a significant peak of free mRNA. Therefore, LPS regulates the expression of MHC class II molecules at translational level in B cells, in addition to the transcriptional control. The actual mechanism implies changes of translation initiation rates, as shown by an increase ribosome loading in polysome gradients.