IgE-ANTIGEN COMPLEXES ENHANCE FcFR AND la EXPRESSION BY MURINE B LYMPHOCYTES

Receptors for the Fc portion of Igs were first identified on lymphocytes in 1970 (1), and later differentiated on the basis oftheir selective affinity for various Ig classes. Fc receptors for IgE (FcsR) are found on a variety of human (2, 3) and rodent (4) cells and can be categorized on the basis oftheir affinity for IgE. High-affinity FcCR (FcsR-I) found on mast cells and basophils (5) clearly mediate allergic degranulation . However, the moderate-affinity FcsR (FcsR-II) present on macrophage/monocytes (6), eosinophils (7), and lymphocytes (2, 8) is less well characterized . The role that lymphocyte FcsRII plays in the regulation of the immune system is the object ofmuch recent study (9-22) . Current evidence supports a model whereby the interaction between IgE and its receptor initiates a cascade of events that give rise to increased FcsR expression and, ultimately, control of IgE production . However, little is known of the consequences of IgE-FcsR interaction as they apply to events that are not directly involved with IgE regulation, such as modulation of other surface molecules on FcsRbearing cells . Indeed, the surprisingly high numbers of FcsR+ lymphocytes, including at least 50% of B cells from BALB/c mouse spleen (23), suggest that the IgE system might participate in immune regulation outside of the limited role to which it has been traditionally ascribed . Additionally, little attention has been directed to the influence of antigen-mediated crosslinking ofFcsR bound IgE molecules particularly as it relates to the role(s) of FcsR+ B cells in an immune response . One report on murine macrophages showed that immune complexes of IgG or IgE inhibit IFN-y-mediated induction of class II antigens of the MHC (24) . Herein we present data that demonstrate that the efficiency with which monoclonal IgE binds to and enhances the expression of B cell FcsR is substantially increased when IgE is complexed with specific antigen. More importantly, we report for the first time that soluble IgE-antigen complexes potently stimulate the cell surface expression of B cell class II MHC (Ia) antigens, while IgE alone (in the absence of antigen) has little effect . This enhancement of la expression suggests that IgE-antigen complexes may play a more generalized role in immune responses than previously assumed.