RGD Reference Report - Tolerogenic Plasmacytoid Dendritic Cells Control Paracoccidioides brasiliensis Infection by Inducting Regulatory T Cells in an IDO-Dependent Manner. - Rat Genome Database

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Tolerogenic Plasmacytoid Dendritic Cells Control Paracoccidioides brasiliensis Infection by Inducting Regulatory T Cells in an IDO-Dependent Manner.

Authors: Araújo, Eliseu Frank de  Medeiros, Daniella Helena  Galdino, Nayane Alves de Lima  Condino-Neto, Antônio  Calich, Vera Lúcia Garcia  Loures, Flávio Vieira 
Citation: Araújo EF, etal., PLoS Pathog. 2016 Dec 19;12(12):e1006115. doi: 10.1371/journal.ppat.1006115. eCollection 2016 Dec.
RGD ID: 39939072
Pubmed: PMID:27992577   (View Abstract at PubMed)
PMCID: PMC5215616   (View Article at PubMed Central)
DOI: DOI:10.1371/journal.ppat.1006115   (Journal Full-text)

Plasmacytoid dendritic cells (pDCs), considered critical for immunity against viruses, were recently associated with defense mechanisms against fungal infections. However, the immunomodulatory function of pDCs in pulmonary paracoccidiodomycosis (PCM), an endemic fungal infection of Latin America, has been poorly defined. Here, we investigated the role of pDCs in the pathogenesis of PCM caused by the infection of 129Sv mice with 1 x 106 P. brasiliensis-yeasts. In vitro experiments showed that P. brasiliensis infection induces the maturation of pDCs and elevated synthesis of TNF-α and IFN-β. The in vivo infection caused a significant influx of pDCs to the lungs and increased levels of pulmonary type I IFN. Depletion of pDCs by a specific monoclonal antibody resulted in a less severe infection, reduced tissue pathology and increased survival time of infected mice. An increased influx of macrophages and neutrophils and elevated presence of CD4+ and CD8+ T lymphocytes expressing IFN-γ and IL-17 in the lungs of pDC-depleted mice were also observed. These findings were concomitant with decreased frequency of Treg cells and reduced levels of immunoregulatory cytokines such as IL-10, TGF-β, IL-27 and IL-35. Importantly, P. brasilienis infection increased the numbers of pulmonary pDCs expressing indoleamine 2,3-dioxygenase-1 (IDO), an enzyme with immunoregulatory properties, that were reduced following pDC depletion. In agreement, an increased immunogenic activity of infected pDCs was observed when IDO-deficient or IDO-inhibited pDCs were employed in co-cultures with lymphocytes Altogether, our results suggest that in pulmonary PCM pDCs exert a tolerogenic function by an IDO-mediated mechanism that increases Treg activity.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
IDO1Humanparacoccidioidomycosis  ISOIdo1 (Mus musculus)mRNA more ...RGD 
Ido1Ratparacoccidioidomycosis  ISOIdo1 (Mus musculus)mRNA more ...RGD 
Ido1Mouseparacoccidioidomycosis  IEP mRNA more ...RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ido1  (indoleamine 2,3-dioxygenase 1)

Genes (Mus musculus)
Ido1  (indoleamine 2,3-dioxygenase 1)

Genes (Homo sapiens)
IDO1  (indoleamine 2,3-dioxygenase 1)


Additional Information