Early CD69 Expression on Peripheral Blood Lymphocytes from Children with Dengue Hemorrhagic Fever

Green, Sharone; Pichyangkul, Sathit; Vaughn, David W.; Kalayanarooj, Siripen; Nimmannitya, Suchitra; Nisalak, Ananda; Kurane, Ichiro; Rothman, Alan L.; Ennis, Francis A.

doi:10.1086/315072

Cited by 195 publications

(213 citation statements)

References 35 publications

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“…T cell lines also were used to study the IFN-g response of Vd2 2 gd T cells to fibroblasts infected with CMV (19). It was reported that the activation marker CD69 is upregulated on gd T cells during dengue infection (20). However, the extent to which primary human gd T cells can rapidly contribute to the anti-DV response by IFN-g production or cytotoxicity is unknown.…”

mentioning

confidence: 99%

Type I IFNs and IL-18 Regulate the Antiviral Response of Primary Human γδ T Cells against Dendritic Cells Infected with Dengue Virus

Tsai

Liong

Gunalan

et al. 2015

The Journal of Immunology

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Little is known about the cellular mechanisms of innate immunity against dengue virus (DV) infection. Specifically, the γδ T cell response to DV has not been characterized in detail. In this article, we demonstrate that markers of activation, proliferation, and degranulation are upregulated on γδ T cells in PBMC isolated from individuals with acute dengue fever. Primary γδ T cells responded rapidly in vitro to autologous DV-infected dendritic cells by secreting IFN-γ and upregulating CD107a. The anti-DV IFN-γ response is regulated by type I IFN and IL-18 in a TCR-independent manner, and IFN-γ secreting γδ T cells predominantly expressed IL-18Rα. Antagonizing the ATP-dependent P2X7 receptor pathway of inflammasome activation significantly inhibited the anti-DV IFN-γ response of γδ T cells. Overnight priming with IL-18 produced effector γδ T cells with significantly increased ability to lyse autologous DV-infected dendritic cells. Monocytes were identified as accessory cells that augmented the anti-DV IFN-γ response of γδ T cells. Lack of monocytes in culture is associated with lower IL-18 levels in culture supernatant and diminished production of IFN-γ by γδ T cells, whereas addition of exogenous IL-18 restored the IFN-γ response of γδ T cells in monocyte-depleted cocultures with DV-infected DC. Our results indicate that primary γδ T cells contribute to the immune response during DV infection by providing an early source of IFN-γ, as well as by killing DV-infected cells, and suggest that monocytes participate as accessory cells that sense DV infection and amplify the cellular immune response against this virus in an IL-18–dependent manner.

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mentioning

confidence: 99%

Type I IFNs and IL-18 Regulate the Antiviral Response of Primary Human γδ T Cells against Dendritic Cells Infected with Dengue Virus

Tsai

Liong

Gunalan

et al. 2015

The Journal of Immunology

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“…Cytokines that may induce plasma leakage such as interferon g, interleukin (IL) 2, and tumour necrosis factor (TNF) are increased in DHF cases [20,21]. Also, interferon enhances uptake of dengue particles by target cells through increasing Fc cell receptors [22].…”

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confidence: 99%

Pathogenesis of Dengue Haemorrhagic Fever and Its Impact on Case Management

Sellahewa

2013

ISRN Infectious Diseases

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Plasma leakage and intrinsic coagulopathy are the pathological hall marks in dengue haemorrhagic fever (DHF). Viral virulence, infection enhancing antibodies, cytokines and chemical mediators in the setting of intense immune activation are the key players implicated in the pathogenesis of DHF; the exact nature of which is yet to be fully understood. e pathophysiological changes the attended clinical features of plasma leakage necessitate recognition of changing physiological parameters for the early recognition of plasma leakage and appropriate �uid therapy. On the other hand, the changes in the haematological indices resulting from coagulopathy can tempt the clinician to initiate other modalities of therapy. A clearer understanding of the pathogenesis of DHF and the appreciation that both of these fundamental pathological changes share common pathogenic mechanisms would facilitate the appropriateness of management decisions and the early recognition of severe disease. us, thrombocytopaenia, reduced �brinogen, and prolonged partial thromboplastin time early in the disease course connoted severe disease and attended plasma leakage rather than clinical bleeding. e detection of plasma cytokine pro�le by a multiple bead immunoassay could also complement clinical parameters in predicting severe disease early in the disease course. us, MIP-indicates good prognosis while IFN-portends severe disease.

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“…The timing of expression of CD69 in this cohort was consistent with previous reports. 13 While Akondy et al 39 reported that CD38, HLA-DR and Ki-67 are specific markers of activation when present in combination, there were a significant proportion of cells that expressed only CD38. Friberg et al 33 found lower intensity of CD38 expression on influenza tetramer-positive cells compared with A11-NS3 133-142 tetramer-positive cells during DENV infection.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have used a number of cell surface markers to phenotype CD8 + T cells in DENV infection. 12,13,26,33,38 We included a diverse panel of surface markers including some that have not previously been studied in DENV infection, such as CD71. The timing of expression of CD69 in this cohort was consistent with previous reports.…”

Section: Discussionmentioning

confidence: 99%

“…[11][12][13] Several studies have reported associations between specific HLA class I alleles and disease severity; these epidemiological links provide additional support for a role of CD8 + T cells in contributing to clinical outcome. [14][15][16][17] HLA-B57 has been associated with slow progression following HIV infection, the clearance of acute HCV infection [18][19][20] and is strongly associated with a number of type 2 idiosyncratic adverse drug reactions.…”

Section: M U N O L O G Y O R I G I N a L A R T I C L Ementioning

confidence: 90%

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Distinct activation phenotype of a highly conserved novel HLA‐B57‐restricted epitope during dengue virus infection

et al. 2013

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SummaryVariation in the sequence of T-cell epitopes between dengue virus (DENV) serotypes is believed to alter memory T-cell responses during second heterologous infections. We identified a highly conserved, novel, HLA-B57-restricted epitope on the DENV NS1 protein. We predicted higher frequencies of B57-NS1 26-34 -specific CD8 + T cells in peripheral blood mononuclear cells from individuals undergoing secondary rather than primary DENV infection. However, high tetramer-positive T-cell frequencies during acute infection were seen in only one of nine subjects with secondary infection. B57-NS1 26-34 -specific and other DENV epitopespecific CD8 + T cells, as well as total CD8 + T cells, expressed an activated phenotype (CD69 + and/or CD38 + ) during acute infection. In contrast, expression of CD71 was largely limited to DENV epitope-specific CD8 + T cells. In vitro stimulation of cell lines indicated that CD71 expression was differentially sensitive to stimulation by homologous and heterologous variant peptides. CD71 may represent a useful marker of antigen-specific T-cell activation.

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Early CD69 Expression on Peripheral Blood Lymphocytes from Children with Dengue Hemorrhagic Fever

Cited by 195 publications

References 35 publications

Type I IFNs and IL-18 Regulate the Antiviral Response of Primary Human γδ T Cells against Dendritic Cells Infected with Dengue Virus

Type I IFNs and IL-18 Regulate the Antiviral Response of Primary Human γδ T Cells against Dendritic Cells Infected with Dengue Virus

Pathogenesis of Dengue Haemorrhagic Fever and Its Impact on Case Management

Distinct activation phenotype of a highly conserved novel HLA‐B57‐restricted epitope during dengue virus infection

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