Interleukin-4 bias differentiation of Trypanosoma cruzi-infected mice B cells to the memory pathway and restrains their fratricide: Fas ligand down-regulation and class II-transactivator up-regulation

ACOSTA RODRIGUEZ EV; ZUÑIGA EI; MONTES CL; GRUPPI A

JOURNAL OF LEUKOCYTE BIOLOGY

Año: 2003 p. 127 - 136

0741-5400

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.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.