Cellular chemotaxis and chemokinesis play important roles in many biological processes. Most continuum mathematical models for these regulatory mechanisms are based on the model of Keller & Segel (1971 a, b), in which cells respond directly to the local concentration of extracellular chemical. We have developed a new model which reflects the receptor-based mechanisms underlying chemical control of cell motion. Our model consists of three coupled partial differential equations, and we use the Boyden chamber (millipore) assay to compare it with a simpler model based on the Keller-Segel approach. The predictions of our model capture the key qualitative features of the experimental data, whereas the simpler model only does so when appropriate functional forms are chosen for the dependence of the transport coefficients on chemical concentration. Using experimental data on the variation of receptor kinetic parameters with temperature, we use our model to predict the effect of decreasing the temperature on both the "leading front" and "migrated cell" measurements taken from Boyden chamber assays. Our results show that changes in the kinetic parameters play a key role in controlling the temperature dependence of cell chemotaxis and chemokinesis.