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The Journal of Immunology, 1998, 160: 1297-1303.
Copyright © 1998 by The American Association of Immunologists

Internalization of Chlamydia by Dendritic Cells and Stimulation of Chlamydia-Specific T Cells1

David M. Ojcius2,*, Yolanda Bravo de Alba{dagger}, Jean M. Kanellopoulos{dagger}, Ray A. Hawkins{ddagger}, Kathy A. Kelly{ddagger}, Roger G. Rank{ddagger} and Alice Dautry-Varsat*

* Unité de Biologie des Interactions Cellulaires, CNRS 1960, and {dagger} Unité de Biologie Moléculaire du Gène, INSERM 277, Institut Pasteur, Paris, France; and {ddagger} Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205

Chlamydia species are the causative agents of trachoma, various forms of pneumonia, and the most common sexually transmitted diseases. Although the infection cycle has been extensively characterized in epithelial cells, where the Chlamydia entry-vacuoles avoid fusion with host-cell lysosomes, the cellular immune response has received less attention. Moreover, despite the abundant presence of dendritic cells (DC) in the sites of infection, the interaction between Chlamydia and DC has never been studied. We observe that DC kill Chlamydia trachomatis and Chlamydia psittaci. The chlamydiae are internalized by the DC in a nonspecific manner through macropinocytosis, and the macropinosomes fuse subsequently with DC lysosomes expressing MHC class II molecules. The interaction induces maturation of the DC, since presentation of an exogenous Ag is severely inhibited after a 1-day incubation, although chlamydial Ags are still presented and recognized by Chlamydia-specific CD4+ T cells. Thus, DC most likely play a role in initiating the T cell response in vivo and could potentially be used in adoptive transfer therapies to vaccinate against Chlamydia.




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