Activated T-lymphocytes express class I molecules which are hyposialylated compared to other lymphocyte populations

Landolfi, Nicholas F.; Cook, Richard G.

doi:10.1016/0161-5890(86)90057-x

Cited by 54 publications

(37 citation statements)

References 34 publications

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“…However, it is possible that an oseltamivir-sensitive endogenous sialidase acts on a substrate other than GSLs to regulate antiviral immunity. For instance, it is known that activated T cells have increased sialidase activity and also have hyposialyated MHC class I molecules (12,26). In our experimental system, oseltamivir treatment had no effect on ex vivo lung mononuclear cell sialidase activity induced by RSV infection (data not shown).…”

Section: Discussionmentioning

confidence: 59%

“…Because T cells activated in vitro have increased endogenous sialidase activity and RSV infection induces a robust T cell response in the lungs of BALB/c mice, we hypothesized that RSV infection would increase endogenous sialidase activity in lung inflammatory cells in vivo (11)(12)(13). Lung mononuclear cells were isolated from mock-infected and RSV-infected mice 6 d.p.i.…”

Section: Rsv Infection Induces Endogenous Sialidase Activity In the Lungmentioning

confidence: 99%

“…One hypothesis is that endogenous sialidases act on GSLs to modulate raft GSL content and cell signaling (9,10). Activation of T cells in vitro induces sialidase gene expression and activity (11)(12)(13). Various GSLs are implicated as targets of endogenous sialidases (9 -11, 13, 14).…”

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confidence: 99%

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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

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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.

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Section: Discussionmentioning

confidence: 59%

Section: Rsv Infection Induces Endogenous Sialidase Activity In the Lungmentioning

confidence: 99%

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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

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“…The induced enzyme is targeted to the plasma membrane and is responsible for processing different molecules expressed on the cell surface, resulting in their hyposialylation [Chen et al, 1997]. Among those molecules are surface antigen-presenting proteins, such as MHC class I, which are required to render T cells responsive to antigen presenting cells [Landolfi and Cook, 1986], and G M3 -ganglioside, which modulates Ca 2+ immobilization and regulates IL4 production [Chen et al, 2000]. In activated B cells, sialidase participates in converting the so-called vitamin D3-binding protein into a macrophage activating factor (MAF) [Yamamoto and Kumashiro, 1993;Naraparaju and Yamamoto, 1994;Yamamoto and Naraparaju, 1996a,b].…”

Section: Future Prospectsmentioning

confidence: 99%

“…Sialidase is overexpressed during the activation of T cells, B cells, macrophages, and neutrophils [Landolfi et al, 1985;Landolfi and Cook, 1986;Cross and Wright, 1991] (N. Stamatos, private communication). The induced enzyme is targeted to the plasma membrane and is responsible for processing different molecules expressed on the cell surface, resulting in their hyposialylation [Chen et al, 1997].…”

Section: Future Prospectsmentioning

confidence: 99%

Molecular pathology of NEU1 gene in sialidosis

Poupětová²,

et al. 2003

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Communicated by Mark H. PaalmanLysosomal sialidase (EC 3.2.1.18) has a dual physiological function; it participates in intralysosomal catabolism of sialylated glycoconjugates and is involved in cellular immune response. Mutations in the sialidase gene NEU1, located on chromosome 6p21.3, result in autosomal recessive disorder, sialidosis, which is characterized by the progressive lysosomal storage of sialylated glycopeptides and oligosaccharides. Sialidosis type I is a milder, late-onset, normosomatic form of the disorder. Type I patients develop visual defects, myoclonus syndrome, cherry-red macular spots, ataxia, hyperreflexia, and seizures. The severe early-onset form, sialidosis type II, is also associated with dysostosis multiplex, Hurler-like phenotype, mental retardation, and hepatosplenomegaly. We summarize information on the 34 unique mutations determined so far in the sialidase gene, including four novel missense and one novel nonsense mutations found in two Czech and two French sialidosis patients. The analysis of sialidase mutations in sialidosis revealed considerable molecular heterogeneity, reflecting the diversity of clinical phenotypes that make molecular diagnosis difficult. The majority of sialidosis patients have had missense mutations, many of which have been expressed; their effects on activity, stability, intracellular localization, and supramolecular organization of sialidase were studied. A structural model of sialidase allowed us to localize mutations in the sialidase molecule and to predict their impact on the tertiary structure and biochemical properties of the enzyme. Hum Mutat 22:343-352,

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Desialylation of Peripheral Blood Mononuclear Cells Promotes Growth of HIV-1

et al. 1997

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Activation of peripheral blood CD4+ helper T lymphocytes establishes a permissive state for growth of HIV-1. Activated T lymphocytes expressed increased sialidase (neuraminidase) activity and were hyposialylated. Treatment of freshly isolated peripheral blood mononuclear cells (PBMCs) with microbial neuraminidase (NANase) or phytohemagglutinin (PHA) prior to infection at low multiplicity with T cell line-adapted HIV-1IIIB resulted in production of large amounts of p24 antigen and reverse transcriptase. In contrast, neither viral component was detected in the medium of mock-treated cells infected at a similar multiplicity through 21 days in culture. The titer of a stock solution of HIV-1IIIB was 1.4 +/- 0.18 log10 greater in NANase-treated PBMCs than in mock-treated cells; the titer was similarly raised 1.5 to 1.76 +/- 0.18 log10 in PHA-treated cells. Growth of the primary isolate HIV-1(91/US/056) was also enhanced in NANase-treated PBMCs; the titer of a stock solution of HIV-1(91/US/056 was 1.0 +/- 0.16 log10 greater in NANase-treated PBMCs than in mock-treated cells 7 days after infection. No enhancement of viral growth in PBMCs was detected when NANase was heat-inactivated or specifically inhibited with 2,3-dehydro-2-desoxy-N-acetyl-neuraminic acid prior to use. Treatment of PBMCs with NANase did not alter the distribution of lymphocyte subsets nor change the density of CD4 antigen per cell after 7 days in culture. Whereas PHA treatment of PBMCs was mitogenic, pretreatment with NANase was not; the amount of [3H]thymidine incorporated into DNA and culture growth characteristics were similar for NANase- and mock-treated cells. Thus, desialylation of PBMCs promoted a permissive state for growth of HIV-1 without affecting the rate of DNA synthesis or relative number of target CD4+ cells.

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Activated T-lymphocytes express class I molecules which are hyposialylated compared to other lymphocyte populations

Cited by 54 publications

References 34 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

Molecular pathology of NEU1 gene in sialidosis

Desialylation of Peripheral Blood Mononuclear Cells Promotes Growth of HIV-1

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