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3 - MHC class I and II pathways for presentation and cross-presentation of bacterial antigens

from I - Dendritic cells and their role in immunity

Published online by Cambridge University Press:  12 August 2009

By
Laurence Bougnères-Vermont  and
Pierre Guermonprez
Edited by
Maria Rescigno
Maria Rescigno
Affiliation:
European Institute of Oncology, Milan
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Summary

DENDRITIC CELLS PRIME ANTI-BACTERIAL CD4+ AND CD8+ T CELLS IN VIVO

It is now widely accepted that dendritic cells (DCs) are crucially required for the priming of T cell responses. Major histo-compatibility complex (MHC) class I and class II presentation pathways ensure the priming of CD8+ and CD4+ T cell, respectively. They thus represent major checkpoints for the induction of adaptative protective immunity toward intracellular bacteria. In this chapter, we will focus on the basic cell biology and physiological regulation of these pathways in the context of bacterial infection. In accordance with the literature, we will refer to “cross presentation” for MHC class I pathways involved in the presentation of non cytosolic antigens.

Listeria, Mycobacteria and Salmonella were shown to actually infect DCs in situ. Some studies have addressed the capacity of DCs purified from infected animals to activate in vitro T cells specific for bacteria-encoded antigens. Intravenous infection of mice with Salmonella and with Mycobacterium bovis BCG (bacillus Calmette-Guérin) leads to the infection of both spleen DC subsets (CD8α− CD11c+ and CD8α+ CD11c+). Both subsets display some MHC class I and II complexes formed after the processing of bacteria-encoded antigens. Bacterial infection may also promote apoptosis, resulting in the delivery of bacterial antigens to DCs upon the phagocytosis of infected apoptotic bodies (see Section 3.5).

Whatever may be the mechanism (infection or dead cells cross presentation), the absolute requirement of DCs to induce anti-bacterial T cell priming was elegantly demonstrated in the Listeria model.

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Dendritic Cell Interactions with Bacteria , pp. 51 - 78
Publisher: Cambridge University Press
Print publication year: 2007

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