Expression of Toll-like receptors on antigen-presenting cells in patients with falciparum malaria

Loharungsikul, Somying; Troye‐Blomberg, Marita; Amoudruz, Petra; Pichyangkul, Sathit; Yongvanitchit, Kosol; Looareesuwan, Sornchai; Mahakunkijcharoen, Yuvadee; Sarntivijai, Suphannee; Khusmith, Srisin

doi:10.1016/j.actatropica.2007.08.002

Cited by 42 publications

(36 citation statements)

References 25 publications

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“…The increased TNF responses reported in the present study concur with increased PBMC TNF production (plus IL-1␤, IL-6, and IL-10) upon TLR1/2 and TLR4 stimulation after experimental P. falciparum sporozoite infection (27). The upregulation of TLR expression may explain the increased TNF production, since acute malaria increases mDC and monocyte TLR2 and TLR4 expression (28,45). Our IL-12 data support previous reports of absent TLR responses in healthy CD1c ϩ mDC after stimulation by a single TLR (i.e., TLR2, -3, -4, -7, -8, or -9) (9).…”

Section: P Falciparum Compromised Cd86 Expression On Cd1csupporting

confidence: 81%

Profoundly Reduced CD1c ⁺ Myeloid Dendritic Cell HLA-DR and CD86 Expression and Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage Malaria Infection

et al. 2016

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dDendritic cells (DCs) are sentinels of the immune system that uniquely prime naive cells and initiate adaptive immune responses. CD1c (BDCA-1) myeloid DCs (CD1c ؉ mDCs) highly express HLA-DR, have a broad Toll-like receptor (TLR) repertoire, and secrete immune modulatory cytokines. To better understand immune responses to malaria, CD1c؉ mDC maturation and cytokine production were examined in healthy volunteers before and after experimental intravenous Plasmodium falciparum infection with 150-or 1,800-parasite-infected red blood cells (pRBCs). After either dose, CD1c؉ mDCs significantly reduced HLA-DR expression in prepatent infections. Circulating CD1c ؉ mDCs did not upregulate HLA-DR after pRBC or TLR ligand stimulation and exhibited reduced CD86 expression. At peak parasitemia, CD1c؉ mDCs produced significantly more tumor necrosis factor (TNF), whereas interleukin-12 (IL-12) production was unchanged. Interestingly, only the 1,800-pRBC dose caused a reduction in the circulating CD1c؉ mDC count with evidence of apoptosis. The 1,800-pRBC dose produced no change in T cell IFN-␥ or IL-2 production at peak parasitemia or at 3 weeks posttreatment. Overall, CD1c؉ mDCs are compromised by P. falciparum exposure, with impaired HLA-DR and CD86 expression, and have an increased capacity for TNF but not IL-12 production. A first prepatent P. falciparum infection is sufficient to modulate CD1c ؉ mDC responsiveness, likely contributing to hampered effector T cell cytokine responses and assisting parasite immune evasion.

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Section: P Falciparum Compromised Cd86 Expression On Cd1csupporting

confidence: 81%

Profoundly Reduced CD1c ⁺ Myeloid Dendritic Cell HLA-DR and CD86 Expression and Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage Malaria Infection

et al. 2016

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“…Interleukin-10 (IL-10) plays an important role in the immune regulation of malaria infection (12,(17)(18)(19). In fact, IL-10 deficiency results in extreme pathology (20).…”

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confidence: 99%

Immune Activation and Regulation in Simian Immunodeficiency Virus-Plasmodium fragile-Coinfected Rhesus Macaques

Trott

Richardson

Hudgens

et al. 2013

J Virol

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“…P. falciparum primes human TLR responses toward a higher cytokine profile both in vitro and in vivo [30]. Patients with severe and mild malaria showed increased surface expression of TLR-2 and TLR-4 on CD14 + monocytes and myeloid dendritic cells [31]. Pre-incubation of peripheral blood mononuclear cells with P. falciparum-infected red blood cells enhances responsiveness to TLR ligands [32].…”

Section: The Genomic Factors Associated With Vitamin D In Malariamentioning

confidence: 99%

The role of Vitamin D in malaria

Lương

Nguyễn

2015

J Infect Dev Ctries

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An abnormal calcium-parathyroid hormone (PTH)-vitamin D axis has been reported in patients with malaria infection. A role for vitamin D in malaria has been suggested by many studies. Genetic studies have identified numerous factors that link vitamin D to malaria, including human leukocyte antigen genes, toll-like receptors, heme oxygenase-1, angiopoietin-2, cytotoxic T lymphocyte antigen-4, nucleotide-binding oligomerization domain-like receptors, and Bcl-2. Vitamin D has also been implicated in malaria via its effects on the Bacillus CalmetteGuerin (BCG) vaccine, matrix metalloproteinases, mitogen-activated protein kinase pathways, prostaglandins, reactive oxidative species, and nitric oxide synthase. Vitamin D may be important in malaria; therefore, additional research on its role in malaria is needed.

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Expression of Toll-like receptors on antigen-presenting cells in patients with falciparum malaria

Cited by 42 publications

References 25 publications

Profoundly Reduced CD1c ⁺ Myeloid Dendritic Cell HLA-DR and CD86 Expression and Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage Malaria Infection

Profoundly Reduced CD1c ⁺ Myeloid Dendritic Cell HLA-DR and CD86 Expression and Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage Malaria Infection

Immune Activation and Regulation in Simian Immunodeficiency Virus-Plasmodium fragile-Coinfected Rhesus Macaques

The role of Vitamin D in malaria

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Expression of Toll-like receptors on antigen-presenting cells in patients with falciparum malaria

Cited by 42 publications

References 25 publications

Profoundly Reduced CD1c + Myeloid Dendritic Cell HLA-DR and CD86 Expression and Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage Malaria Infection

Profoundly Reduced CD1c + Myeloid Dendritic Cell HLA-DR and CD86 Expression and Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage Malaria Infection

Immune Activation and Regulation in Simian Immunodeficiency Virus-Plasmodium fragile-Coinfected Rhesus Macaques

The role of Vitamin D in malaria

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Profoundly Reduced CD1c ⁺ Myeloid Dendritic Cell HLA-DR and CD86 Expression and Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage Malaria Infection

Profoundly Reduced CD1c ⁺ Myeloid Dendritic Cell HLA-DR and CD86 Expression and Increased Tumor Necrosis Factor Production in Experimental Human Blood-Stage Malaria Infection