The present data strongly suggest that the pleomorphic lymphoid proliferation
characteristic of W.M. represents the proliferation of a clone of B cells
which continues to mature and differenciate into 1gM secreting plasma cells.’5
It is thus not surprising that the 5.1gM shares the eventual anti-IgG antibody
activity of the secreted serum 1gM, and a similar situation appears likely
in cold agglutinin disease. It is worth noting that 5.1gM persists- on 1gM
secreting plasma cells, as already shown in normal rabbit.5 The presence of
S.Ig on 1gM plasma cells may be of interest with respect to the chronology
of the immune response. Conversely, we did not find S.Ig on the plasma
cells of some of the studied cases of classical IgG or IgA myeloma, nor in the
three cases of pleomorphic lymphoid proliferation with serum monoclonal IgG
or IgA herein reported. These latter cases demonstrate that the syndrome of B
cell proliferation with persistent maturation into plasma cells is not restricted
to macroglobulinemia and can also occur for IgG or IgA carrying lymphocytes.
Another situation, i.e., “nonsecreting macroglobulinemia,” can also
occur in this syndrome since the present study includes a patient with all
the features of W.M., including the results of the immunofluorescence studies,
but with no monoclonal serum 1gM. This situation is similar to that of
nonsecreting myeloma where we have previously demonstrated the presence
of an apparently unreleased intracytoplasmic monoclonal 1g.33