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The Expression of MHC Class II Genes in Macrophages Is Cell Cycle Dependent¹

Departament de Fisiologia (Biologia del Macròfag), Facultat de Biologia and Fundació August Pi i Sunyer, Campus de Bellvitge, Universitat de Barcelona, Barcelona, Spain

Using different drugs, we stopped the cell cycle of bone marrow-derived macrophages at different points. After IFN- stimulation, macrophages arrested at the G₁ phase of the cell cycle did not increase cell surface expression of the MHC class II IA. This inhibition is specific, because, under the same conditions, IFN- induces the expression of Fc receptors and the inducible NO synthase mRNA. Treatments that inhibit macrophage proliferation by blocking the cell cycle at the G₁ phase, such as adenosine, forskolin, or LPS, blocked the IFN- induction of IA. Under IFN- treatment, the steady-state levels of IA and IA mRNA did not increase in cells arrested at the G₁ phase and the half-life of the MHC mRNA was not modified. These data suggest that the cell cycle modulation of IFN--induced MHC II gene expression occurs at the transcriptional level. The expression of the class II transactivator mRNA induced by IFN- was also blocked when macrophages were arrested at the G₁ phase of the cell cycle, suggesting that the lack of IFN- response occurs at the early steps of MHC class II expression. Finally, macrophages arrested at the G₁ phase showed increased basal levels of cell surface IA due to an increase of the translational efficiency. These data show that the expression of MHC class II genes is regulated by the cell cycle.

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