Fc gamma RII expression in resting and activated B lymphocytes
- PMID: 2550246
- DOI: 10.1002/eji.1830190805
Fc gamma RII expression in resting and activated B lymphocytes
Abstract
In this report, we analyze the expression of the type II receptor for the Fc region of IgG (Fc gamma RII) in resting and lipopolysaccharide (LPS)-activated murine B lymphocytes. Fc gamma RII is encoded by two genes, alpha and beta. The beta gene encodes two mRNA, beta 1 and beta 2, which are generated by alternative splicing. Using an S1 nuclease protection assay, we found that resting and activated B lymphocytes express predominantly the beta 1 transcript. Very low levels of the beta 2 mRNA were detected in this assay, while no expression of the alpha transcript could be detected. Quantitative Northern blot analysis showed that the amount of Fc gamma RII beta mRNA was increased 9-fold in LPS-activated B lymphocytes. The expression of Fc gamma RII during the various phases of B cell activation was then studied by immunofluorescence using the monoclonal antibody 2.4G2. LPS stimulation induced an increase of the Fc gamma RII cellular pool as well as of its expression at the surface of B lymphocytes. The rise in Fc gamma RII surface expression occurred after the induction of class II antigens (Ia) and before transferrin receptor induction. Fc gamma RII expression was found to be enhanced during the G1 phase of the cell cycle since (a) only large cells (i.e. those that had entered the G1 phase) expressed an increased amount of Fc gamma RII and (b) blocking the entry of activated cells into the S phase (with the ion channel blocker quinine) did not affect the Fc gamma RII induction by LPS. Furthermore, only B cell activators that induced cells to enter into G1 [LPS and F(ab')2 anti-IgM antibodies, but not interleukin 4] caused an increase in the expression of Fc gamma RII. These results show that the increase in the membrane expression of Fc gamma RII occurs during the early G1 phase, establishing it as a marker for the entry of B lymphocytes into the cell cycle.
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