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Review
. 2014 May 13:5:212.
doi: 10.3389/fimmu.2014.00212. eCollection 2014.

Tumor immunotherapy: lessons from autoimmunity

Christian Maueröder  1 , Luis Enrique Munoz  1 , Ricardo Alfredo Chaurio  1 , Martin Herrmann  1 , Georg Schett  1 , Christian Berens  2
Affiliations
Review

Tumor immunotherapy: lessons from autoimmunity

Christian Maueröder et al. Front Immunol. .
No abstract available

Keywords: autoimmunity; cell death; danger model; immunotherapy; tumor microenvironment; tumor vaccination.

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Figures

Figure 1
Figure 1
The dual role of cell death in tumor tolerance/immunity. (A) Role of apoptotic cells in formation of the tumor microenvironment. Apoptotic cells (AC) are mainly taken up by monocytes (MC; yellow) and alternatively activated macrophages (M2; green). Upon phagocytosis of ACs, MCs, and classically activated macrophages (M1, red) get polarized toward an M2-phenotype. M2-macrophages participate in tissue remodeling and angiogenesis and via secretion of anti-inflammatory cytokines (TGF-β, IL-10), inhibit M1-activation of macrophages and shift TH1-responses toward the TH2-phenotype. (B) Tumor-supportive effects of apoptotic cells are abrogated by Annexin-A5. Annexin-A5 (yellow circles on secondary necrotic cells) inhibits swift clearance of apoptotic cells, leading to progression of ACs into secondary necrosis. Secondary necrotic cells (SNEC) are mainly taken up by MCs, classically activated macrophages and dendritic cells (DC; red). Upon phagocytosis of SNEC, MCs get polarized toward the M1-phenotype. Phagocytosis of SNEC by DCs leads to antigen presentation and priming of T cells. Classically activated macrophages secrete inflammatory cytokines (TNF-α, IL-1β) and induce TH1-responses via IL-12.
See this image and copyright information in PMC

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