We have previously reported that TGF-β1 in combination with IL-2 or IL-5 increases the synthesis of IgA isotype by LPS-activated mouse spleen B cells. However, there are no conclusive reports on the role of cytokines including TGF-β1 in the
gut-associated lymphoid tissue (GALT). In this study, we investigated the effect of TGF-β1, IL-2, IL-5, and IL-10 on the IgA synthesis by B cell population from GALT, e.g. Peyer's patch(PP), mesenteric lymph node (ML), and lamina propria (LP).
Unstimulated whole PP cells readily secreted a substantial amount of IgA isotype. There was no increase in IgA isotype synthesis when TGF-β1 and/or IL-2 was added to culture in the presence of LPS. The same is true for sIgA PP B cells. Under any
circumstances, no significant amount of IgM and IgG1 isotypes was produced by PP cell population. On the other hand, TGF-β1 IN combination with IL-2 significantly increased total IgA production and secreting cell number by LPS-activated ML B
cells, but
not IgM or IgG1isotype. This observation was similar to what we made previously for spleen B cells although the IgA enhancing effect of TGF-β1 and IL-2 on the former was less than the latter.
B cells from LP, which is known to be a terminal site for IgA secretion in the intestinal tract, responded weakly to TGF-β1 and IL-2 in the secretion of IgA isotype. IgM or IgG1 isotypes was not produced at all by this cell population.
In conclusion, the results from the present study indicate that most PP B cells are already committed to IgA cells, eventually homing to LP. Further, ML B cells are partially committed to IgA B cells, suggesting that most of IgA B cells are
derived
from
PP, and the rest of B cells (uncommitted) are migrate from either systemic circulation or peritoneal cavity.
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