Triggering of Dendritic Cell Responses after Exposure to Activated, but Not Resting, Apoptotic PBMCs

Johansson, Ulrika; Walther-Jallow, Lilian; Smed-Sörensen, Anna; Spetz, Anna-Lena

doi:10.4049/jimmunol.179.3.1711

Cited by 50Immunotherapy and Immune ResponsesPhagocytosis and Immune RegulationImmune Response and Inflammation

Triggering of Dendritic Cell Responses after Exposure to Activated, but Not Resting, Apoptotic PBMCs

Johansson, Ulrika, Walther-Jallow, Lilian, Smed-Sörensen, Anna, Spetz, Anna-Lena·2007·The Journal of Immunology

DOI 10.4049/jimmunol.179.3.1711

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Abstract

Dendritic cells (DCs) can be activated by signaling via pathogen receptors, by interaction with activated T cells or by exposure to inflammatory mediators. Clearance of apoptotic cells by DCs is generally considered a silent event that is not associated with an inflammatory response. Necrotic cell death, in contrast, leads to induction of inflammation. However, emerging data challenge the view of apoptotic cells as inherently nonimmunogenic. In this study, we report that the activation state of the apoptotic cell may determine whether the exposed DC becomes activated and rendered proficient in Ag presentation. We show that coculture with activated, but not resting, apoptotic PBMCs leads to up-regulation of surface expression of the costimulatory molecules CD80, CD83, and CD86 in human DCs as well as release of proinflammatory cytokines. Furthermore, we show that DCs exposed to allogeneic, activated apoptotic PBMCs induce proliferation and IFN-γ production in autologous T cells. Together, these findings show that activated apoptotic PBMCs per se provide an activation/maturation signal to DCs, suggesting that activated apoptotic PBMCs possess endogenous adjuvant properties.

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T cells that succumb to activation-induced cell death promote tolerance through stimulation of regulatory CD8+ T cells.
“An interesting contrast is with the effect of T cells that succumb to activation-induced cell death, which promote tolerance through the stimulation of regulatory CD8+ T cells30.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [30]

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Activated Apoptotic Cells Induce Dendritic Cell Maturation via Engagement of Toll-like Receptor 4 (TLR4), Dendritic Cell-specific Intercellular Adhesion Molecule 3 (ICAM-3)-grabbing Nonintegrin (DC-SIGN), and β2 Integrins
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Authors: Johansson, U., Walther-Jallow, L., Smed-Sörensen, A., & Spetz, A.-L.
Affiliations: Karolinska University Hospital (SE)
Department of Medicine, Center for Infectious Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge , Stockholm ,
ORCID: Johansson, Ulrika
Spetz, Anna-Lena
Venue: The Journal of Immunology
Publisher: Oxford University Press (OUP)
Published: 2007-08-01
Volume: 179
Issue: 3
Pages: 1711-1720
ISSN: 0022-1767 (ISSN-L)
1550-6606
DOI: 10.4049/jimmunol.179.3.1711
OpenAlex: W1525166884
Cited by: 50
References: 73
Citations by year: 2023: 1 · 2022: 3 · 2020: 1 · 2019: 2 · 2017: 1 · 2016: 1 · 2015: 2 · 2014: 7 · 2013: 5 · 2012: 4
FWCI: 2.34
Type: journal article
Language: en
Open access: closed
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: The Journal of Immunology (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: dendritic cell activation, apoptotic cells, dendritic cell maturation, costimulatory molecules, CD80, CD83, CD86, inflammatory cytokines, T cell proliferation, interferon-gamma, allogeneic cells, antigen presentation, necrosis
MeSH terms: Cell Differentiation, Cell-Free System, Cells, Cultured, Dendritic Cells, Humans, Interferon-gamma, Isoantigens, Leukocytes, Mononuclear, Monocytes, Necrosis, Phagocytosis, T-Lymphocyte Subsets, Resting Phase, Cell Cycle, Apoptosis, Coculture Techniques, Cell Proliferation

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Triggering of Dendritic Cell Responses after Exposure to Activated, but Not Resting, Apoptotic PBMCs

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