Source: http://www.asmscience.org/content/book/10.1128/9781555815523.ch20
Timestamp: 2019-04-21 08:57:47+00:00

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Transmission electron microscopy images of lungs of mice with A. fumigatus infection. Mice were intratracheally injected with viable Aspergillus conidia 2 h before being processed for transmission electron microscopy. (A) Conidia are internalized by phagocytic cells with characteristics of DC morphology, as judged by the numerous cytoplasmic extensions and abundant cytoplasm present in the alveolar spaces. Magnification, × 12,000. (B) Through emission of pseudopods, DC engulf conidia and make contact with the epithelial barrier (arrow). Magnification, ×8,000. (C) DC with engulfed conidia and free conidia migrate through invaginated epithelial cells (arrow). Magnification, × 8,000. (D) DC with engulfed conidia are present within the alveolar septal wall. Magnification, × 12,000. Reproduced from Bozza et al. (2002b) with permission of the publisher.
Transmission electron microscopy images of phagocytosis of A. fumigatus by DC. Fetal skin-derived murine DC were incubated with live unopsonized A. fumigatus conidia (A to D) or hyphae (E to G) for 1 h (A and E) or 3 h (B, C, D, F, and G) before processing for transmission electron microscopy. (A) Conidial engulfment through coiling phagocytosis. Magnification, × 20,000. (B) Conidia inside the cells 3 h later. Magnification, ×12,000. (C and D) Conidia are emanating thick projections (C; magnification, ×30,000) through which they make contact with mitochondria (D, arrow; magnification, ×35,000). (E and F) Hyphal uptake through zipper-type phagocytosis at 1 h after infection (E; magnification, ×8,000) and inside the cells (F; magnification, ×8,000). (G) Hyphae in partially degraded forms at 3 h after exposure (arrows). Magnification, ×8,000. Reproduced from Bozza et al. (2002b) with permission from the publisher.
Encounter of DC subsets with A. fumigatus leads to a distinct outcome. Under steady-state conditions, in the absence of accompanying danger signals in the lung, inhaled conidia and small hyphal fragments are picked up by lung DC, which take the cargo antigen to draining lymph nodes, where the close interaction with naïve Th cells results in the activation of distinct Th cell responses ( Bozza et al., 2002b ). Conventional CD11c+ DC and CD11c+ B200+ IDO+ pDC sense fungi in a morphotype-dependent manner through the engagement of distinct receptors ( Bozza et al., 2002b; , Romani et al., 2006 ). This translates into downstream signaling events that differentially affect cytokine production and Th cell activation. PAMP, pathogen-associated molecular pattern; MyD88, Drosophila melanogaster myeloid differentiation primary response gene 88; TRIF, Toll/IL-1R domain-containing adaptor inducing IFN-β.
Exploiting DC for transplantation tolerance and concomitant pathogen clearance in hematopoietic transplantation. The figure shows the relative contributions of murine DC subsets to antifungal priming and alloantigen tolerization upon adoptive transfer in vivo in HSCT mice with aspergillosis ( Romani et al., 2006 ). Specialization and complementarity in priming and tolerization by the different DC subsets is shown. Whereas CD11c+ DC activate Th1 cells and concomitant inflammatory toxicity, CD11c+ B220+ IDO+ DC fulfilled the requirement for (i) Th1/Treg antifungal priming, (ii) tolerization toward alloantigens, and (iii) diversion from alloantigen-specific to antigen-specific T-cell responses in the presence of donor T lymphocytes. Interestingly, Ta1, known to modulate human pDC functions through TLR9, affected mobilization and tolerization of pDC by activating the IDO-dependent pathway, and this resulted in Treg development and tolerization ( Romani et al., 2006 ). Thus, transplantation tolerance and concomitant pathogen clearance can be achieved through the therapeutic induction of antigen-specific Tregs via instructive immunotherapy with pathogen- or TLR-conditioned donor DC. GVHD, graft-versus-host disease.
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