Antigens capable of cross-linking the BCR are preferentially captured, proc
essed and presented to MHC-class-II-restricted T cells. Cross-linking antig
ens initiate tyrosine-kinase-dependent pathways that accelerate the deliver
y of antigen-receptor complexes to specialized late-endocytic processing co
mpartments. Accelerated trafficking is mediated by the recruitment of signa
ling molecules required for transience through specific checkpoints along t
he endocytic pathway.