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In addition, OX40L inhibited IL-10 production in differentiated IL-10 producing regulatory T cells [37].
Previous studies have shown that IL-10 producing regulatory T cells were able to prevent or suppress autoimmune diseases.
Future investigation will analyze a possible impact of increased IL-10 production by CD83Tg B cells in vivo, especially if CD83Tg B cells share features with IL-10 producing regulatory B cells [33] [35] that have been described to be beneficial in various autoimmune disease models such as the recovery from EAE in resistant B6 mice [36].
These observations are easily explained by our model since experiments also show that natural regulatory T cells can induce the differentiation of precursor T cells into IL-10 producing regulatory T cells [43] and thus act as an initial regulatory force to maintain tolerance.
Conversely, several experiments have shown that DCs treated with IL-10, a cytokine secreted by regulatory T cells such as type 1 regulatory T cells, are rendered immature and induce the differentiation of CD4 cells into IL-10 producing regulatory T cells [15] [17].
The present review will therefore focus exclusively on the IL-10 producing regulatory B cell subset.
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That is, certain of the newly expressed genes produced regulatory proteins that turned on transcription of their own genes as they worked on others, as well.
Regulatory T cells (Treg) are known to produce regulatory cytokines like IL-10 and TGFβ.
In parallel, the thymus produces regulatory T cells whose main action is in the periphery control of development, trafficking and proliferation of responder T cells.
Indeed, at steady state, the gut is home to a large number of lymphocytes that have the capacity to produce regulatory (IL-10 or TGF-b) cytokines.
However, while spatial interaction is necessary for some regulatory elements, like enhancers, to execute their function, transcript-producing regulatory elements do not necessarily need to interact directly with the genes to affect their transcription.
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