Professional APCs engage in continuous endocytosis, and in the absence of pathogens, they display at their surface class I and class II MHC molecules loaded with peptides derived from self proteins. In the presence of pathogens, the TLRs on these cells are activated, inducing the APCs to become motile: they detach from the surrounding substratum and start to migrate in the direction of the draining lymph node, following the directional cues provided by chemokines. An activated dendritic cell, for example, reduces its rate of antigen acquisition, up-regulates the activity of endosomal and lysosomal proteases, and increases the transfer of class II MHC–peptide complexes from the loading compartments to the cell surface. Finally, activated professional APCs up-regulate expression of the co-stimulatory molecules CD80 and CD86, which will allow them to activate T cells more effectively. The initial contact of a professional APC with a pathogen thus results in its migration to the draining lymph node in a state that is fully capable of activating a naive T cell. Antigen is displayed in the form of peptide-MHC complexes, co-stimulatory molecules are abundantly present, and cytokines are produced that assist in setting up the proper differentiation program for the T cells to be activated.
Antigen-laden dendritic cells engage antigen-specific T cells, which respond by proliferating and differentiating. The cytokines produced in the course of this priming reaction determine whether a CD4-expressing T cell will polarize toward an inflammatory or a classic helper T cell phenotype. If engagement occurs via class I MHC molecules, a CD8-expressing T cell may develop from a precursor cytotoxic T cell into a fully active cytotoxic T cell. Activated T cells are motile and move through the lymph node in search of B cells or enter the circulation to execute effector functions elsewhere in the body.