Chapter 20 : Dendritic Cells in Infection and Allergy

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Innate and adaptive immune responses act to generate the most effective form of immunity for protection against . The inflammatory allergic manifestations that follow contact with or inhalation of spp. all constitute compelling evidence for the pathogenic role of T-cell dysreactivity in fungal diseases. Allergy is an overzealous Th2 response to environmental airborne allergens. The association of persistent inflammation with intractable infection is common in nonneutropenic patients after allogeneic hematopoietic stem cell transplantation (HSCT) as well as in those with allergic fungal diseases. This chapter highlights how the remarkable functional plasticity of dendritic cells (DC) in response to the fungus may accommodate the activation of different mechanisms of immunity and can be exploited for the deliberate targeting of cells and pathways of protective cell-mediated immunity and for the identification of candidate fungal vaccines. The inflammatory/anti-inflammatory state of DC is strictly controlled by the metabolic pathway involved in tryptophan catabolism and mediated by indoleamine 2,3-dioxygenase (IDO). Antigenspecific proliferation was induced by conventional DC, more than pDC, from healthy donors but not by DC from HSCT patients. These results suggest that human pDC are fully competent at inducing IFN-γ-/IL-10-producing cells in response to the fungus in vitro and are defective at early stages after HSCT.

Citation: Romani L. 2009. Dendritic Cells in Infection and Allergy, p 247-261. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch20
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Image of Figure 1.
Figure 1.

Transmission electron microscopy images of lungs of mice with infection. Mice were intratracheally injected with viable 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 with permission of the publisher.

Citation: Romani L. 2009. Dendritic Cells in Infection and Allergy, p 247-261. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch20
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Image of Figure 2.
Figure 2.

Transmission electron microscopy images of phagocytosis of by DC. Fetal skin-derived murine DC were incubated with live unopsonized 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 with permission from the publisher.

Citation: Romani L. 2009. Dendritic Cells in Infection and Allergy, p 247-261. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch20
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Image of Figure 3.
Figure 3.

Encounter of DC subsets with 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 ( ). Conventional CD11c DC and CD11c B200 IDO pDC sense fungi in a morphotype-dependent manner through the engagement of distinct receptors ( ). This translates into downstream signaling events that differentially affect cytokine production and Th cell activation. PAMP, pathogen-associated molecular pattern; MyD88, myeloid differentiation primary response gene 88; TRIF, Toll/IL-1R domain-containing adaptor inducing IFN-β.

Citation: Romani L. 2009. Dendritic Cells in Infection and Allergy, p 247-261. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch20
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Image of Figure 4.
Figure 4.

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 ( ). 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 ( ). 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.

Citation: Romani L. 2009. Dendritic Cells in Infection and Allergy, p 247-261. In Latgé J, Steinbach W (ed), and Aspergillosis. ASM Press, Washington, DC. doi: 10.1128/9781555815523.ch20
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