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Interleukin-2 (IL-2) stimulates both activated CD4 + and CD8 + T cells to proliferate. IL-2 signals through an identical receptor complex and promotes the same dose-dependent phosphorylation of the canonical transcription factor STAT5 in both cell types. Despite this, CD8 + T cells enter the S phase earlier and proliferate to a greater extent than do CD4 + T cells in response to IL-2. We identified distinct IL-2 signaling dynamics in CD4 + and CD8 + T cells. In IL-2-stimulated CD8 + T cells, STAT5 phosphorylation increased rapidly and was sustained for 6 hours. In contrast, CD4 + T cells had a biphasic response, with maxima at 15 min and 2 to 4 hours after stimulation. Both cell types required vesicular trafficking, but only CD4 + T cells required new protein synthesis to maintain high phosphorylation of STAT5. Two subunits of the IL-2 receptor, IL-2Rβ and IL-2Rγ, were twice as abundant in CD8 + T cells than in CD4 + T cells. Reduction of IL-2Rβ abundance by 50% was sufficient to convert CD8 + T cells to a CD4 + T cell-like signaling pattern and delay S phase entry. These results suggest that the larger pool of IL-2Rβ chains in CD8 + T cells is required to sustain IL-2 signaling and contributes to the quantitatively greater proliferative response to IL-2 relative to that of CD4 + T cells. This cell type-specific difference in IL-2Rβ abundance appears to tune responses, potentially preventing extensive, autoimmune proliferation of CD4 + T cells, while still enabling sufficient proliferation of CD8 + T cells to control viral infections.

IL-2Rβ abundance differentially tunes IL-2 signaling dynamics in CD4 + and CD8 + T cells

IL-2Rβ abundance differentially tunes IL-2 signaling dynamics in CD4 ⁺ and CD8 ⁺ T cells