These results suggest that IL-21 signaling drives the differentiation of short-lived effector CD8(+) T cells (KLRG1(high) CD127(low)) from early effector CD8(+) T cells (KLRG1(low) CD127(low)) but does not inhibit the exhaustion of CD8(+) T cells following BCG infection in mice.
results demonstrate that in the setting of lupus-like CD4 T cell-driven B cell hyperactivity IL-21 signaling on Ag-specific donor CD8 T cells is critical for CTL effector maturation whereas a lack of IL-21R downregulates CTL responses that would otherwise limit B cell hyperactivity and autoantibody production
Ly108 expression distinguishes subsets of invariant NKT cells that help autoantibody production and secrete IL-21 from those that secrete IL-17 in lupus prone NZB/W mice.
IL-21 signaling to B cells is essential for the development of all classical disease manifestations but IL-21 signaling also supports the expansion of central memory CD8(+) suppressor cells and broadly represses the cytokine activity of CD4(+) T cells.
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