A proteasome-dependent, TAP-independent pathway for cross-presentation of phagocytosed antigen.

Nawel Merzougui, Roland Kratzer, Loredana Saveanu, Peter van Endert

Institut National de la Santé et de la Recherché Médicale, Unité 1013, Paris 75015, France.

EMBO reports 2011 Dec

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Major histocompatibility complex (MHC) class I cross-presentation is thought to involve two pathways, one of which depends on both the TAP transporters and the proteasome and the other on neither. We found that preincubation of TAP-deficient dendritic cells at low temperature increases the density of MHC class I at the surface and fully restores cross-presentation of phagocytosed antigen, but not of soluble antigen internalized through receptors. Restoration of cross-presentation by TAP-deficient cells requires antigen degradation by the proteasome. Thus, TAP might mainly be required for recycling cell surface class I molecules during cross-presentation of phagocytosed antigens. Furthermore, phagosomes-but not endosomes-seem to have a TAP-independent mechanism to import peptides generated by cytosolic proteasome complexes.

Citation

Nawel Merzougui, Roland Kratzer, Loredana Saveanu, Peter van Endert. A proteasome-dependent, TAP-independent pathway for cross-presentation of phagocytosed antigen. EMBO reports. 2011 Dec;12(12):1257-64