No abstract

Endocytosis of the major histocompatibility complex (MHC)-encoded class I and class II molecules has been the subject of recent investigations. Class I molecules, which are key elements in T cell-mediated cytotoxicity, are differentially endocytosed by different cell types. Fibroblasts internalize their class I molecules via uncoated cell surface vesicles and tubular invaginations when these molecules are cross-linked with multivalent ligands. T lymphocytes internalize their class I molecules spontaneously, but B lymphocytes do not internalize them at all. Here we describe a morphological investigation of the mechanism by which class I molecules are endocytosed by T lymphocytes. We show that, unlike fibroblasts, T lymphocytes spontaneously internalize 20-40% of their class I molecules in a process involving coated pits and coated vesicles. Thus, the endocytic pathway of class I molecules in T lymphocytes is similar to those of other more classical cell-surface receptors involved in receptor-mediated endocytosis. In contrast, the same class I molecules remained on the cell surface in B lymphocytes. These data show that class I molecules are differentially regulated in T and B lymphocytes and fibroblasts.

We evaluated MHC class I‐ and II‐restricted presentation of exogenous antigen by mouse bone marrow‐derived dendritic cells (DC) and splenic B cells. DC presented to class I‐restricted transgenic T cells femtomolar concentrations of antigens from liposomes targeted to the IgG Fc receptor. Targeting these liposomes to surface immunoglobulin did not permit B cells to stimulate class I‐restricted responses. Nevertheless, both DC and B cells presented antigen from liposomes targeted to these same receptors with equivalent efficiency to class II‐restricted T cells. Acquisition of the capacity to present class II‐restricted antigens required shorter periods of differentiation of DC than presentation of exogenous class I‐restricted antigens. The latent period for class I‐restricted presentation of exogenous antigen by DC could not be shortened by exposing them to lipopolysaccharide, double‐stranded RNA or antibody to CD40. Class I presentation depended on expression of the TAP1 transporter. Our data are consistent with the existence of a regulated transport process present in DC which can convey exogenous antigen from endocytic vesicles to the cytosol.