What Determines an Antigen‐Specific IgE Isotypic Response?—A Hypothesis

Summary Two models to account for an antigen‐specific IgE isotypic response are proposed. Both models assume a first‐tiered IgE production induced by antigen and IL‐4; however, the processed IgE or Ag IgE immune complexes stimulate Tɛ cells differently in the two models. In Model I. we propose that Tɛ cells express conventional T‐cell receptors which recognize IgE isotypic determinants. Model IA proposes that IgE fragments are processed and recognized along with class II MHC molecules, and Tɛ cell preferentially act on antigen‐activated IgE‐committed Tɛ cells via recognition o! processed membrane IgE determinants but not antigens; thus Tɛ cells are in principle capable of modulating non‐antigen‐specific polyclonal IgE responses. Model IB proposes that IgE function as a class‐restriction determinant for nominal antigens analogous to that of class II molecules, and Tɛ cells exert stringent antigen‐specific IgE isotypic responses by recognizing nominal antigens restricted to IgE, Tɛ cells thus exert antigen‐specific and IgE concerted immunoregulation. and do not participate in modulating polyclonal IgE production. Model II proposes a heterotypic interaction of IgE with a cell interaction receptor (or IgE Fc receptor) on T cells, Tɛ cells modulate antigen‐specific IgE isotypic responses via ligation with IgE antigen immune complexes on B‐cell surface; thus. Tɛ cells in principle contribute to polyclonal IgE responses.