T cells and dendritic cells (DCs) must interact to initiate immune responses against invading pathogens. Immature DCs, located at sites of antigen entry such as the gut mucosa, are specialized for antigen capture but lack the ability to activate T cells. As they mature, DCs migrate to peripheral lymphoid organs where they lose the ability to capture antigen but acquire the capacity to activate naïve T cells carrying receptors for that antigen (1). Thus, DCs have all of the features that are essential for the initiation of T cell immunity.

Newly activated CD4 T cells commit early to a pathway of differentiation that results in the formation of two functionally distinct T cell subsets: T helper 1 (T H 1) and T H 2. T H 1 and T H 2 cells differ in the cytokines they secrete (2) and the type of response (3) they elicit in target cells expressing cytokine-specific receptors. The activation of the appropriate T cell subset is critical for providing protective immunity against a variety of pathogens: T H 1 immunity protects against intracellular parasites such as Leishmania, and T H 2 immunity protects against extracellular pathogens such as helminths. The current theory to explain the selectivity of T cell responses postulates that cytokines secreted by neighboring cells drive resting naïve T cells down a particular differentiation pathway. However, a study by Rissoan and colleagues on page 1183 of this issue (4) challenges aspects of this model by suggesting that DCs not only provide a common set of signals to initiate clonal expansion of T cells but also provide T cells with selective signals leading to either T H 1 or T H 2 immunity (see the figure).