Abstract
MHC class II‐mediated antigen presentation by B lymphocytes or dendritic cells (DC) initiates CD4^+^ T lymphocyte activation. In B lymphocytes, MHC class II peptide presentation has been characterised by recruitment of MHC class II, F‐actin and lipid rafts to the B cell–T cell immunological synapse. We now show that MHC class II engagement in B lymphocytes induced lipid raft‐independent Rho and Rac activation and that inhibition of either Rho‐GTPase activation or actin polymerisation in the B cell abrogated T cell activation without altering B cell–T cell conjugate formation. Short‐hairpin RNA studies excluded a role for the Cdc42 effector Wiskott–Aldrich syndrome protein. In contrast, antigen presentation by DC was Rho‐GTPase‐independent although actin was recruited to the DC–T cell interaction site. Moreover, actin depolymerisation in the DC significantly increased T cell activation without altering the number of DC–T cell conjugates. Finally we show that stable recruitment of HLA‐DR to the site of the immunological synapse is not a uniform observation in DC and demonstrate reduced HLA‐DR expression at the site of microtubule organising centre polarization. Therefore although actin accumulates in DC and B lymphocytes at the immunological synapse with antigen‐specific T lymphocytes, this does not reflect comparable functional roles of their actin cytoskeletons in antigen presentation.