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Production from CD3intIL-2Rß+ T Cells1
*
Department of Immunology and Medical Zoology, and
Laboratory of Host Defenses, Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
SJL mice are known for their poor IgE production upon helminth
infection. In this study, we have demonstrated that SJL standard B
cells (85% IgM+ or B220+), prepared by
complement-mediated T cell lysis, failed to proliferate and to produce
IgE and IgG1 in response to LPS plus IL-4 in vitro. This diminished IgE
production was restored by anti-IL-12 and enhanced by additional
treatment with anti-IL-18, suggesting active suppression by the
cells that produce IL-12 and IL-18. Indeed, SJL standard B cells were
contaminated with Mac-1+ cells. Therefore, we removed
macrophages by passing standard B cells through a Sephadex G-10 column
(G10). Resultant cells (95% IgM+), designated as G10-B
cells, responded to LPS and IL-4 by their proliferation and
differentiation. G-10 treatment markedly diminished the proportion of
B220- cells and Mac-1+ cells in SJL standard B
cells. Furthermore, addition of SJL B220- cells dose
dependently and MHC independently inhibited LPS plus IL-4-induced B
cell growth and IgE production in SJL and BALB/c B cells.
B220- cells in SJL standard B cells contained
Mac-1+ cells (51%) and Fas ligand+
CD4-CD8- double-negative
CD3intIL-2Rß+ T cells (26%). Thus, IL-12 and
IL-18 produced by LPS-stimulated Mac-1+ cells stimulate
this unique subpopulation of T cells to produce IFN-
, which in
combination with Fas ligand, inhibits IgE production from the B cells.
Our present results indicate that Mac-1+ cells and
double-negative CD3intIL-2Rß+ T cells,
uniquely abundant in the spleens of SJL mice, inhibit IgE production,
indicating their new role in IgE response.
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