DEFECTIVE IGE PRODUCTION BY SJL MICE IS LINKED TO THE ABSENCE OF CD4(-CELLS THAT PROMPTLY PRODUCE INTERLEUKIN-4(), NK1.1(+) T)

SJL mice produce little or no IgE in response to polyclonal stimulatio n with anti-IgD antibody and fail to express interleukin 4 (IL-4) mRNA in the spleen 5 days after injection of anti-IgD, in contrast to othe r mouse strains that produce substantial amounts of IgE and IL-4. Beca use IL-4 is critical in IgE production, the possibility that SJL mice are poor IgE producers because their naive T cells fail to differentia te into IL-4 producers must be seriously considered. IL-4 itself is th e principal factor determining that naive T cells develop into IL-4 pr oducers. A major source of IL-4 for such differentiation is a populati on of CD1-specific CD4(+) T cells that express NK1.1. These cells prod uce IL-4 within 90 min of anti-CD3 injection. T cells from SJL mice fa il to produce IL-4 in response to injection of anti-CD3. Similarly, SJ L T cells and CD4(+) thymocytes do not produce IL-4 in response to acu te in vitro stimulation. SJL T cells show a marked deficiency in CD4() cells that express the surface receptors associated with the NK1.1() T-cell phenotype. This result indicates that the SJL defect in IgE a nd IL-4 production is associated with, and may be due to, the absence of the CD4(+), NK1.1(+) T-cell population.