A cellular automata (CA) model has been built to study the interaction between T-helper subset cells in a secondary lymphoid organ during chronic and acute infection. The T(H) subset cells interacted via short range cytokine-like factors, each cell type producing an autocrine factor and another factor which suppressed the development and proliferation of the other T(H) cell type. A cell death term was also included such that T cells not restimulated by antigen within a certain time died to be replaced with new naive cells. The important parameters in the model were the antigen density entering the lymph node and the propensity of the antigens to induce naive T cells down a specific T(H) subset pathway. Many features of the response of the CA were found to match those seen in infections known to induce T(H) subset polarization. For example, it could be seen that T(H) cell subset polarization arose as a natural consequence of the dynamic competition between T(H)1 and T(H)2 cytokines to induce or suppress proliferation and was driven by the antigen produced by the pathogen.