Calcium signaling is crucial for T cell activation. T cell receptor activation leads to the down-stream generation of IP3 which opens IP3 receptors on the membrane of the endoplasmic reticulum (ER), resulting in an initial small rise in cytoplasmic Ca2+. T cells do not have sufficiently large Ca2+ stores to sustain Ca2+ elevation and therefore require additional Ca2+ influx through the voltage-independent Ca2+ channel CRAC, which is encoded by the ORAI1 or CRACM1 gene and is activated by STIM1, which “senses” decrease in ER Ca2+ content. However, CRAC can only bring in Ca2+ at negative membrane potentials. This potential is generated by the potassium channels Kv1.3 and KCa3.1 which drive the membrane potential back to -60 mV and facilitate Ca2+ entry for the duration of T cell activation ultimately leading to cytokine production and T cell proliferation. While there have been tremendous strides acquiring biophysical data on the implicated ion channels this data has not been integrated into a dynamic model. A computer model has been developed that integrates the available data on calcium signaling in T lymphocytes and that can be utilized to illustrate and theoretically probe T cell activation. The design is implemented in LabVIEW and can be run on a PC. The program allows free reign over the cell's environment and channel characteristics. The interface provides visualization of IP3 production, membrane potential, charge flow and open probability of the aforementioned channels. We suggest this program as a tool for identifying pharmaceutical targets for intervening with immune cell activation and as a teaching aid for immunology, physiology and cell signaling.