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Affinity and dose of T cell receptor (TCR) interaction with antigens govern the magnitude of CD4+ T cell responses, but questions remain regarding the quantitative translation of TCR engagement into downstream signals. We find that while the response of mouse CD4+ T cells to antigenic stimulation is bimodal, activated cells exhibit analog responses proportional to signal strength. Gene expression output reflects TCR signal strength, providing a signature of T cell activation. Expression changes rely on a pre-established enhancer landscape and quantitative acetylation at AP-1 binding sites. Finally, we show that graded expression of activation genes depends on ERK pathway activation, suggesting that an ERK-AP-1 axis plays an important role in translating TCR signal strength into proportional activation of enhancers and genes essential for T cell function. DOI: http://dx.doi.org/10.7554/eLife.10134.001, eLife digest T helper cells recognize and respond to bacteria, viruses and other invading microbes and thus play a central role in the adaptive immune system. These cells have a receptor on their surface that binds to fragments of proteins – known as oligopeptides – from the microbes that have been digested and presented on the surfaces of other immune cells. Once active, T helper cells multiply, grow and release signals that regulate genes in other cells to promote immune responses. Previous studies suggest that a T helper cell’s response is binary – that is, either on or off. However, this does not explain how the strength of the T cell response to infection can vary. Allison et al. used a technique called high-throughput sequencing to examine the activity of genes in T helper cells from mice that had been genetically engineered to only produce one type of T cell receptor. For the experiments, the T cells were exposed to various concentrations of different peptides known to bind either well or poorly to the receptor. Allison et al. found that, once activated, the response of an individual T cell was not binary, but instead was related to the strength of the signal it received through its receptor. Further experiments showed that although a subset of the genes activated in T helper cells do respond in a binary fashion, the activities of many other genes involved in immune responses and cell metabolism were related to the strength of the signal from the receptor. This “analog” gene activation depends on the level of activity of the MAP kinase signaling pathway. Together, Allison et al.’s findings help us to understand how T cells are able to fine-tune immune responses to invading microbes. The next challenge will be to investigate the mechanisms underlying binary and analog gene activity in T cells. DOI: http://dx.doi.org/10.7554/eLife.10134.002