In:
The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 1_Supplement ( 2012-05-01), p. 49.5-49.5
Abstract:
Immune responses are modified by a diverse and abundant repertoire of carbohydrate structures on cell surface, which is known as the “glycome”. We herein report a colitis-associated glycome & lt;CAG & gt;that is created on the colonic, but not systemic, memory CD4+T cells under intestinal inflammatory conditions. Through gene screening approaches, we found that CAG represents an immature core-1 O-glycan that is created through the decreased expression of an enzyme, core-2 β1,6-N-acetylglucosaminyltransferase & lt;C2GnT & gt;1 that is responsible for the production of core-2 O-glycan branch through an addition of GlcNAc to a core-1 O-glycan. Indeed, restoration of C2GnT1 expressions using T-cell-specific C2GnT transgenic mice abolished the inflammation-induced development of CAG on colonic CD4+T cells. Functionally, the CAG promoted the proliferation of memory CD4+T cells, resulting in the exacerbation of colitis. Mechanistically, CAG induced the “super rafts” formation on memory CD4+T cells, which provide a place for initiating the signaling machinery for T cell activation. Indeed, the CAG contributed for sustaining the activation of protein kinase C θ, a key signaling molecule for T cell activation. These findings suggest that a specific glycome, which is created on memory CD4+T cells under intestinal inflammatory conditions, leads to further exacerbation of diseases by promoting memory T cell expansion.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.188.Supp.49.5
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2012
detail.hit.zdb_id:
1475085-5
detail.hit.zdb_id:
3056-9
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