Functional Evaluation of Activation-dependent Alterations in the Sialoglycan Composition of T Cells

Naito-Matsui, Yuko; Takada, Shuhei; Kano, Yoshinobu; Iyoda, Tomonori; Sugai, Manabu; Shimizu, Akira; Inaba, Kayo; Nitschke, Lars; Tsubata, Takeshi; Oka, Shogo; Kozutsumi, Yasunori; Takematsu, Hiromu

doi:10.1074/jbc.m113.523753

Cited by 30 publications

(22 citation statements)

References 59 publications

(69 reference statements)

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“…Interestingly, it has been reported that both resting T-and B-cells preferentially carry Neu5Gc in ␣-2,6-linkage. Cell activation, however, results in marked changes in the glycosylation pattern, including a shift to Neu5Ac in ␣-2,3-linkage (36,66). As a result, expression of Siglec-1 and Siglec-E ligands is enhanced on these lymphocytes.…”

Section: Discussionmentioning

confidence: 99%

Mouse Siglec-1 Mediates trans-Infection of Surface-bound Murine Leukemia Virus in a Sialic Acid N-Acyl Side Chain-dependent Manner

Erikson

Wratil

Frank

et al. 2015

Journal of Biological Chemistry

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Background: Human Siglec-1 mediates HIV trans-infection by interaction with virion-associated sialylated gangliosides. Results: Here, Siglec-1 on mouse macrophages mediated trans-infection of surface-bound MLV. This could be inhibited by biosynthetic modification of sialic acids' N-acyl side chain in virus-producer cells. Conclusion:The N-acyl side chain is a critical determinant of Siglec-1-dependent MLV trans-infection. Significance: Glycoengineering allows manipulation of sialic acid-dependent virus/receptor interactions.

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Section: Discussionmentioning

confidence: 99%

Mouse Siglec-1 Mediates trans-Infection of Surface-bound Murine Leukemia Virus in a Sialic Acid N-Acyl Side Chain-dependent Manner

Erikson

Wratil

Frank

et al. 2015

Journal of Biological Chemistry

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“…Another possibility where unmasking of CD22 on GC B-cells could make an impact is in B-T cell interactions (32). Indeed, several studies have suggested that CD22 can modulate B-T cell interactions (12,(32)(33)(34)(35). Decreased cis ligands on GC B-cells could also be a means of modulating the interactions between CD22 and the BCR to regulate B-cell signaling or endocytosis.…”

Section: Discussionmentioning

confidence: 99%

“…As coordinated movement of GC B-cells between the light zone and dark zone of the GC is critical in the selection process (14), CD22 could participate in this migration. Another possibility where unmasking of CD22 on GC B-cells could make an impact is in B-T cell interactions (32). Indeed, several studies have suggested that CD22 can modulate B-T cell interactions (12,(32)(33)(34)(35).…”

Section: Discussionmentioning

confidence: 99%

Unmasking of CD22 Co-receptor on Germinal Center B-cells Occurs by Alternative Mechanisms in Mouse and Man

Macauley¹,

Kawasaki²,

Peng³

et al. 2015

Journal of Biological Chemistry

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Background: Changes in glycosylation on germinal center B-cells have the potential to influence CD22. Results: CD22 is unmasked on germinal centers due to loss of its preferred ligand. Conclusion: Different biosynthetic mechanisms in mice and humans down-regulate the preferred CD22 ligand on germinal center B-cells. Significance: Conserved unmasking of CD22 on germinal center B-cells from mice and humans suggests an important role for CD22 in the germinal center.

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“…Over the last years, several papers have demonstrated the importance of differential sialylation for CD8 + T cells with respect to their maturation ( Moody et al, 2001 ; Naito-Matsui et al, 2014 ), activation ( Pappu and Shrikant, 2004 ), and cytotoxic responses ( Sadighi Akha et al, 2006 ). However, few studies provided insights into the impact of surface sialylation of CD8 + T cells on infectious diseases.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Cell Sialoglycophenotype: A Stylish Mechanism Adopted by Trypanosoma cruzi to Ensure Its Persistence in the Infected Host

et al. 2016

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Trypanosoma cruzi, the etiological agent of Chagas disease exhibits multiple mechanisms to guarantee its establishment and persistence in the infected host. It has been well demonstrated that T. cruzi is not able to synthesize sialic acids (Sia). To acquire the monosaccharide, the parasite makes use of a multifunctional enzyme called trans-sialidase (Tc-TS). Since this enzyme has no analogous in the vertebrate host, it has been used as a target in drug therapy development. Tc-TS preferentially catalyzes the transfer of Sia from the host glycoconjugates to the terminal β-galactopyranosyl residues of mucin-like molecules present on the parasite’s cell surface. Alternatively, the enzyme can sialylate/re-sialylate glycoconjugates expressed on the surface of host cells. Since its discovery, several studies have shown that T. cruzi employs the Tc-TS activity to modulate the host cell sialoglycophenotype, thus favoring its perpetuation in the infected vertebrate. In this review, we summarize the dynamic of host/parasite sialoglycophenotype modulation, highlighting its role in the subversion of host immune response in order to promote the establishment of persistent chronic infection.

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Functional Evaluation of Activation-dependent Alterations in the Sialoglycan Composition of T Cells

Cited by 30 publications

References 59 publications

Mouse Siglec-1 Mediates trans-Infection of Surface-bound Murine Leukemia Virus in a Sialic Acid N-Acyl Side Chain-dependent Manner

Mouse Siglec-1 Mediates trans-Infection of Surface-bound Murine Leukemia Virus in a Sialic Acid N-Acyl Side Chain-dependent Manner

Unmasking of CD22 Co-receptor on Germinal Center B-cells Occurs by Alternative Mechanisms in Mouse and Man

Modulation of Cell Sialoglycophenotype: A Stylish Mechanism Adopted by Trypanosoma cruzi to Ensure Its Persistence in the Infected Host

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