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Microparticles released by Listeria monocytogenes-infected macrophages are required for dendritic cell-elicited protective immunity


Zhang, Yi; Zhang, Ruihua; Zhang, Huafeng; Liu, Jing; Yang, Zhuoshun; Xu, Pingwei; Cai, Wenqian; Lu, Geming; Cui, Miao; Schwendener, Reto A; Shi, Huang-Zhong; Xiong, Huabao; Huang, Bo (2012). Microparticles released by Listeria monocytogenes-infected macrophages are required for dendritic cell-elicited protective immunity. Cellular & Molecular Immunology, 9(6):489-496.

Abstract

Interplay between macrophages and dendritic cells in the processing and presentation of bacterial antigens for T-cell immune responses remains poorly understood. Using a Listeria monocytogenes (Lm) infection model, we demonstrate that dendritic cells (DCs) require the support of macrophages to elicit protective immunity against Lm infection. DCs themselves were inefficient at taking up Lm but capable of taking up microparticles (MPs) released by Lm-infected macrophages. These MPs transferred Lm antigens to DCs, allowing DCs to present Lm antigen to effector T cells. MP-mediated Lm antigen transfer required MHC class I participation, since MHC class I deficiency in macrophages resulted in a significant reduction of T-cell activation. Moreover, the vaccination of mice with MPs from Lm-infected macrophages produced strong protective immunity against Lm infection. We here identify an intrinsic antigen transfer program between macrophages and DCs during Lm infection, and emphasize that macrophages also play an essential role in DC-elicited Lm-specific T-cell responses.

Abstract

Interplay between macrophages and dendritic cells in the processing and presentation of bacterial antigens for T-cell immune responses remains poorly understood. Using a Listeria monocytogenes (Lm) infection model, we demonstrate that dendritic cells (DCs) require the support of macrophages to elicit protective immunity against Lm infection. DCs themselves were inefficient at taking up Lm but capable of taking up microparticles (MPs) released by Lm-infected macrophages. These MPs transferred Lm antigens to DCs, allowing DCs to present Lm antigen to effector T cells. MP-mediated Lm antigen transfer required MHC class I participation, since MHC class I deficiency in macrophages resulted in a significant reduction of T-cell activation. Moreover, the vaccination of mice with MPs from Lm-infected macrophages produced strong protective immunity against Lm infection. We here identify an intrinsic antigen transfer program between macrophages and DCs during Lm infection, and emphasize that macrophages also play an essential role in DC-elicited Lm-specific T-cell responses.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Molecular Cancer Research
07 Faculty of Science > Institute of Molecular Cancer Research
Dewey Decimal Classification:570 Life sciences; biology
Language:English
Date:2012
Deposited On:15 Oct 2013 15:01
Last Modified:07 Dec 2017 22:47
Publisher:Chinese Society of Immunology
ISSN:1672-7681
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1038/cmi.2012.33
PubMed ID:23064105

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