Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.53 (sialidase)
 2,694 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently shown that treatment of T cells from aged mice with an endopeptidase specific for O-linked glycoproteins can restore synapse formation and early activation markers to CD4 cells from aged mice. New data show that the sialidase from Clostridium perfringens, but not from Vibrio cholerae, can increase activation of CD4 cells from both old and young mice as measured by calcium signals, expression of CD25 and CD69, and secretion of IL-2. Lectin binding assays showed alterations with age in the levels, accessibility or conformation of multiple glycoproteins on the surface of CD4 cells. While some alterations were due to the accumulation of memory cells with age, others were age sensitive and found exclusively in the naive subset or both naive and memory subsets. Furthermore, analysis of the sialic acid links alpha(2,3)Gal/GalNAc and alpha(2,6)Gal/GalNAc in immunoprecipitated CD43 and CD45 molecules confirm that age alters the glycosylation of specific proteins that regulate TCR interaction with antigen presenting cells. These data support the idea that changes in T cell surface glycosylation could play an important role in immune senescence.
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PMID:Age-associated changes in glycosylation of CD43 and CD45 on mouse CD4 T cells. 1566 24

Decreased binding by the 6C10 auto-antibody serves as a unique marker for CD4+ T cell unresponsiveness after the induction of T cell tolerance in Vbeta8.1 TCR transgenic mice. We further define the nature of the epitope recognized by the 6C10 antibody to be a subset of Thy-1 bearing incompletely sialylated N-linked glycans, and furthermore, we demonstrate that tolerant CD4+ T cells have an increased degree of cell-surface sialylation. To test the significance of the altered glycosylation state identified by the 6C10 auto-antibody in the tolerant CD4+ T cell population, surface sialic acid was cleaved enzymatically. Treatment of purified peripheral CD4+ T cells with Vibrio cholerae sialidase (VCS) leads to increased 6C10 binding, significantly enhances proliferation in the tolerant CD4+ population and corrects defects in phosphotyrosine signaling observed in the tolerant CD4+ T cell. Furthermore, in vivo administration of VCS enhances proliferation in both tolerant and naive CD4+ T cell subsets. These studies suggest that sialylation of glycoproteins on the surface of the CD4+ T cell contributes to the regulation of T cell responsiveness in the tolerant state.
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PMID:Sialylation regulates peripheral tolerance in CD4+ T cells. 1629 58