期刊
JOURNAL OF LEUKOCYTE BIOLOGY
卷 73, 期 1, 页码 127-136出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1189/jlb.0702353
关键词
apoptosis; memory B cell; plasma cell; control mechanism; survival
In the present work, we demonstrate that interleukin (IL)-4 is able to rescue B cells from Trypanosoma cruzi-infected mice, counteracting the strong apoptotic signals that these cells received in vivo. We have observed that IL-4 restrains the apoptosis of immunoglobulin (Ig)M+ and IgG(+) B cells from infected and normal mice without inducing them to proliferate. In addition, IL-4 does not modify the quantity or quality of the antibodies secreted by B cells from infected mice, as it blocks their terminal differentiation to plasma cells and favors memory pathway. It is interesting that the protective effect of IL-4 over B cells from infected mice is mediated, at least partly, by the down-regulation of Fas ligand (FasL) expression, which leads to interference in the apoptosis executed by these B cells through the Fas/FasL death pathway. Accordingly, a marked up-regulation of the FasL gene repressor class II transactivator was observed, suggesting that this would be one mechanism underlying the IL-4-mediated FasL down-regulation.
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