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- W64642009 abstract "All trans-Retinoic acid (RA) is an important regulator for the immune system, but its role in B-cell activation is unclear. To study how RA regulates B-cell activation and early differentiation, we have used a model of purified mouse splenic B cells stimulated by ligation of CD40 (a surrogate of T cell co-stimulation), and treatment with IL-4, a principal Th-2 cytokine, along with the B-cell antigen receptor (BCR). CD40 engagement or IL-4 alone induced B-cell activation indicated by increased cell proliferation, Ig γ1 germline transcripts (γ1 GLT), and surface (s)IgG1 expression, while triple stimulation with anti-CD40/anti-μ/IL-4 synergized to heighten B-cell activation. RA (20 nM) was growth inhibitory for anti-CD40/anti-μ-activated B cells, but did not inhibit cell proliferation in the presence of IL-4. Whereas RA reduced γ1 GLT expression induced by CD40 ligation and IL-4, it up-regulated sIgG1 at both condition. Flow cytometry showed that triple stimulation including RA increased the proportion of mature B cells that were larger in size, had undergone fewer division cycles, and were enriched for γ1 GLT and sIgG1. These results suggest that CD40 and IL-4 may use different signaling pathways at the early phase of B-cell activation. RA regulates B-cell activation in a complex manner, as it inhibited the early cell proliferation and γ1 GLT level, it simultaneously promoted the formation of sIgG1 expressing cells." @default.
- W64642009 created "2016-06-24" @default.
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- W64642009 creator A5078326314 @default.
- W64642009 date "2007-01-01" @default.
- W64642009 modified "2023-09-27" @default.
- W64642009 title "Retinoic acid regulates mouse B‐cell activation and differentiation induced by engagement of CD40, B‐cell antigen receptor and cytokine IL‐4" @default.
- W64642009 doi "https://doi.org/10.1096/fasebj.21.6.a737-c" @default.
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