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Selective inhibition of spontaneous IgE and IgG4 production by
interleukin-8 in atopic patients
H Kimata, I Lindley and K Furusho
Department of Pediatrics, Kyoto University Hospital, Japan.
The effects of interleukin (IL)-8 on spontaneous IgE and IgG4 production in
atopic patients were studied. IL-8 inhibited IgE and IgG4 production by
purified surface (s) IgE+ and sIgG4+ B cells, respectively, while it had no
effect on IgG1, IgG2, IgG3, IgM, IgA1, and IgA2 production by corresponding
sIg+ B cells. The IL-8-induced inhibition was counteracted by IL-6 and
tumor necrosis factor-alpha (TNF-alpha) and was blocked by anti-IL-8
monoclonal antibody (MoAb). Conversely, the addition of anti-IL-6 MoAb and
anti-TNF-alpha MoAb, in the absence of IL-8, inhibited IgE and IgG4
production by sIgE+ and sIgG4+ B cells, respectively. Purified sIgE+ and
sIgG4+ B cells expressed IL-6 receptors (R), TNF-alpha R, and IL-8R, and
they produced IL-6 and TNF-alpha, but not IL-8. IL-8 had no effect on IL-6R
or TNF- alpha R, while it abrogated IL-6 and TNF-alpha production in these
cells. In contrast, slgG1+, slgG2+, slgG2+, slgG3+, slgM+, slgA1+, and
slgA2+ B cells expressed IL-6R and TNF-alpha R but not IL-8R, and they
produced IL-6 and TNF-alpha. IL-8 had no effect on IL-6R and TNF-alpha R,
or on TNF-alpha and IL-6 production in these cells. These results indicate
that IL-8 inhibits spontaneous IgE and IgG4 production in slgE+ and slgG4+
B cells, respectively, by inhibiting the endogenous production of IL-6 and
TNF-alpha.
Volume 85,
Issue 11,
pp. 3191-3198,
06/01/1995
Copyright © 1995 by The American Society of Hematology
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