Intracellular IFN-gamma expression in natural killer cells precedes lung CD8+ T cell recruitment during respiratory syncytial virus infection.

Hussell, Tracy; Openshaw, Peter

doi:10.1099/0022-1317-79-11-2593

Cited by 155 publications

(119 citation statements)

References 40 publications

Supporting

Mentioning

110

Contrasting

Unclassified

Order By: Relevance

“…RSV is the chief cause of bronchiolitis and viral pneumonia in infants. In BALB/c mice, the immune response to primary infection with the A2 strain of RSV is characterized by the influx of IFN-␥-producing T cells in the lung and a robust CTL response (18,19). We now show that RSV increases activated T cell GM1 expression in vivo and induces endogenous sialidase activity in lung mononuclear cells.…”

mentioning

confidence: 66%

See 1 more Smart Citation

Cutting Edge: Oseltamivir Decreases T Cell GM1 Expression and Inhibits Clearance of Respiratory Syncytial Virus: Potential Role of Endogenous Sialidase in Antiviral Immunity

Moore¹,

Michael²,

Zhou³

et al. 2007

The Journal of Immunology

View full text Add to dashboard Cite

The sialoglycosphingolipid GM1 is important for lipid rafts and immune cell signaling. T cell activation in vitro increases GM1 expression and increases endogenous sialidase activity. GM1 expression has been hypothesized to be regulated by endogenous sialidase. We tested this hypothesis in vivo using a mouse model of respiratory syncytial virus (RSV) infection. RSV infection increased endogenous sialidase activity in lung mononuclear cells. RSV infection increased lung CD8+ T cell surface GM1 expression. Activated CD8+ T cells in the lungs of RSV-infected mice were GM1high. Treatment of RSV-infected mice with the sialidase/neuraminidase inhibitor oseltamivir decreased T cell surface GM1 levels. Oseltamivir treatment decreased RSV-induced weight loss and inhibited RSV clearance. Our data indicate a novel role for an endogenous sialidase in regulating T cell GM1 expression and antiviral immunity. Also, oseltamivir, an important anti-influenza drug, inhibits the clearance of a respiratory virus that lacks a neuraminidase gene, RSV.

show abstract

mentioning

confidence: 66%

“…(23). The peak pulmonary T cell response of BALB/c mice to primary RSV infection is 6 -12 d.p.i., and the IFN-␥-expressing CD8 ϩ T cells peak earlier than RSV-specific CD8 ϩ T cells (18,19,24). Thus, 6 d.p.i.…”

Section: Rsv Infection Increases Gm1 Levels On Cd8 ϩ T Cells In the Lungmentioning

confidence: 90%

Cutting Edge: Oseltamivir Decreases T Cell GM1 Expression and Inhibits Clearance of Respiratory Syncytial Virus: Potential Role of Endogenous Sialidase in Antiviral Immunity

Moore¹,

Michael²,

Zhou³

et al. 2007

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…150 Indeed, blocking PD-L1 with a specific-antibody in hRSV-infected BECs, co-cultured with CD8 C T cells, enhances CD8 C T cell effector functions and decreases hRSV gene expression in BECs. 108 In addition, CD8 C T cells may not only be directly influenced by the impairment of the T cell priming by DCs, but also be indirectly affected by the modulation of cytokine environment, as NK cell-derived IFN-g production precedes lung CD8 C T cell recruitment, 109 in a mechanism similar to the Influenza A virus. 110 Also, temporally association has been made between CD8 C T cells and neutrophils, where an important influx of neutrophils to the airways in infants occurs before CD8 C T cells activation.…”

mentioning

confidence: 99%

Aberrant T cell immunity triggered by human Respiratory Syncytial Virus and human Metapneumovirus infection

et al. 2016

View full text Add to dashboard Cite

Human Respiratory syncytial virus (hRSV) and human metapneumovirus (hMPV) are the two major etiological viral agents of lower respiratory tract diseases, affecting mainly infants, young children and the elderly. Although the infection of both viruses trigger an antiviral immune response that mediate viral clearance and disease resolution in immunocompetent individuals, the promotion of long-term immunity appears to be deficient and reinfection are common throughout life. A possible explanation for this phenomenon is that hRSV and hMPV, can induce aberrant T cell responses, which leads to exacerbated lung inflammation and poor T and B cell memory immunity. The modulation of immune response exerted by both viruses include different strategies such as, impairment of immunological synapse mediated by viral proteins or soluble factors, and the induction of pro-inflammatory cytokines by epithelial cells, among others. All these viral strategies contribute to the alteration of the adaptive immunity in order to increase the susceptibility to reinfections.In this review, we discuss current research related to the mechanisms underlying the impairment of T and B cell immune responses induced by hRSV and hMPV infection. In addition, we described the role each virulence factor involved in immune modulation caused by these viruses.

show abstract

“…The most abundant cytokine in clinical specimens from RSVinfected children is IFN-␥, and most RSV infections likely resolve via a typical antiviral Th-1-type response (2). In BALB/c mice, RSV A2 strain infection causes an increase in the number of IFN-␥-producing NK cells in bronchoalveolar lavage fluid (BALF) that precedes the BALF appearance of abundant IFN-␥-producing CD8 cells and cytotoxic T lymphocytes (CTLs) (5)(6)(7). Both CD4 ϩ and CD8 ϩ T cells exacerbate RSV-induced illness and contribute to virus clearance in primary infection of BALB/c mice (8).…”

mentioning

confidence: 99%

Differential Regulation of GM1 and Asialo-GM1 Expression by T Cells and Natural Killer (NK) Cells in Respiratory Syncytial Virus Infection

et al. 2008

View full text Add to dashboard Cite

We previously reported that respiratory syncytial virus (RSV) infection increases lung CD8 ϩ T cell GM1 expression. The related lipid asialo-GM1 (ASGM1) is expressed by T cells in viral infection and by natural killer (NK) cells. The in vivo co-expression of GM1 and ASGM1 by immune cells is not defined. Here we analyzed lung lymphocyte GM1 and ASGM1 expression in RSV-infected mice. GM1 and ASGM1 were coordinately upregulated by activated CD8 ϩ T cells in RSV-infected BALB/c and C57BL/6 mice. In contrast, RSV infection had no effect on constitutively high NK cell GM1 expression, while increasing NK cell ASGM1 expression. GM1 and ASGM1 co-localized in lipid raft structures in NK and CD8 ϩ T cells sorted from the lungs of RSV-infected mice. Anti-ASGM1 Ab treatment of RSV-infected BALB/c mice depleted GM1/ASGM1-expressing NK cells and GM1/ASGM1-expressing T cells, reduced lung IFN-␥ levels, increased viral load, delayed viral clearance, and reduced illness. STAT1 Ϫ/Ϫ mice are more susceptible to RSV replication and disease than wild-type mice. In RSV-infected STAT1 Ϫ/Ϫ mice, anti-ASGM1 Ab altered cytokine levels, but in contrast to BALB/c mice, antibody treatment had no effect on viral load or illness. Taken together, GM1 and ASGM1 expression are differentially regulated by T and NK cells in RSV infection. Also, GM1/ASGM1-expressing cells are important for control of RSV in BALB/c mice, whereas STAT1 Ϫ/Ϫ mice clear RSV by an alternative pathway. 327

show abstract

Intracellular IFN-gamma expression in natural killer cells precedes lung CD8+ T cell recruitment during respiratory syncytial virus infection.

Cited by 155 publications

References 40 publications

Cutting Edge: Oseltamivir Decreases T Cell GM1 Expression and Inhibits Clearance of Respiratory Syncytial Virus: Potential Role of Endogenous Sialidase in Antiviral Immunity

Cutting Edge: Oseltamivir Decreases T Cell GM1 Expression and Inhibits Clearance of Respiratory Syncytial Virus: Potential Role of Endogenous Sialidase in Antiviral Immunity

Aberrant T cell immunity triggered by human Respiratory Syncytial Virus and human Metapneumovirus infection

Differential Regulation of GM1 and Asialo-GM1 Expression by T Cells and Natural Killer (NK) Cells in Respiratory Syncytial Virus Infection

Contact Info

Product

Resources

About