FcγRII expression in resting and activated B lymphocytes

Sebastian Amigorena, Christian Bonnerot, Daniel Choquet, Wolf Herman Fridman, Jean-Luc Teillaud
Eur. J. Immunol.. 1989-08-01; 19(8): 1379-1385
DOI: 10.1002/eji.1830190805

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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.

Auteurs Bordeaux Neurocampus