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*
Department of Internal Medicine, Division of Immunology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, and Veterans Affairs Medical Center, Cincinnati, OH 45220; and
Department of Immunology and Microbiology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814
Injection of mice with a foreign anti-IgD Ab stimulates B
and T cell activation that results in large cytokine and Ab responses.
Because most anti-IgD-activated B cells die before they can be
stimulated by activated T cells, and because IL-4 prolongs the survival
of B cells cultured with anti-Ig, we hypothesized that treatment
with IL-4 at the time of anti-IgD Ab injection would decrease B
cell death and enhance anti-IgD-induced Ab responses. Instead, IL-4
treatment before or along with anti-IgD Ab suppressed IgE and IgG1
responses, whereas IL-4 injected after anti-IgD enhanced IgE
responses. The suppressive effect of early IL-4 treatment on the Ab
response to anti-IgD was associated with a rapid, short-lived
increase in IFN-
gene expression but decreased CD4+ T
cell activation and decreased or delayed T cell production of other
cytokines. We examined the possibilities that IL-4 stimulation of
IFN- production, suppression of IL-1 or IL-2 production, or
induction of TNF-
or Fas-mediated apoptosis could account for
IL-4’s suppressive effect. The suppressive effect of IL-4 was not
reversed by IL-1, IL-2, or anti-TNF- or anti-IFN- mAb
treatment, or mimicked by treatment with anti-IL-2R (CD25) and
anti-IL-2Rß (CD122) mAbs. Early IL-4 treatment failed to inhibit
anti-IgD-induced Ab production in Fas-defective lpr
mice; however, the poor responsiveness of lpr mice to
anti-IgD made this result difficult to interpret. These
observations indicate that exposure to IL-4, while T cells are first
being activated by Ag presentation, can inhibit T cells activation or
promote deletion of responding CD4+ T
cells.
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