Inducible colitis-associated glycome capable of stimulating the proliferation of memory CD4+ T cells

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Inducible colitis-associated glycome capable of stimulating the proliferation of memory CD4+ T cells

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Title: Inducible colitis-associated glycome capable of stimulating the proliferation of memory CD4+ T cells
Author: Nishida, Atsushi; Nagahama, Kiyotaka; Imaeda, Hirotsugu; Ogawa, Atsuhiro; Lau, Cindy W.; Kobayashi, Taku; Hisamatsu, Tadakazu; Preffer, Frederic I.; Mizoguchi, Emiko; Ikeuchi, Hiroki; Hibi, Toshifumi; Fukuda, Minoru; Andoh, Akira; Blumberg, Richard S.; Mizoguchi, Atsushi

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Citation: Nishida, A., K. Nagahama, H. Imaeda, A. Ogawa, C. W. Lau, T. Kobayashi, T. Hisamatsu, et al. 2012. “Inducible colitis-associated glycome capable of stimulating the proliferation of memory CD4+ T cells.” The Journal of Experimental Medicine 209 (13): 2383-2394. doi:10.1084/jem.20112631. http://dx.doi.org/10.1084/jem.20112631.
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Abstract: Immune responses are modified by a diverse and abundant repertoire of carbohydrate structures on the cell surface, which is known as the glycome. In this study, we propose that a unique glycome that can be identified through the binding of galectin-4 is created on local, but not systemic, memory CD4+ T cells under diverse intestinal inflammatory conditions, but not in the healthy state. The colitis-associated glycome (CAG) represents an immature core 1–expressing O-glycan. Development of CAG may be mediated by down-regulation of the expression of core-2 β1,6-N-acetylglucosaminyltransferase (C2GnT) 1, a key enzyme responsible for the production of core-2 O-glycan branch through addition of N-acetylglucosamine (GlcNAc) to a core-1 O-glycan structure. Mechanistically, the CAG seems to contribute to super raft formation associated with the immunological synapse on colonic memory CD4+ T cells and to the consequent stabilization of protein kinase C θ activation, resulting in the stimulation of memory CD4+ T cell expansion in the inflamed intestine. Functionally, CAG-mediated CD4+ T cell expansion contributes to the exacerbation of T cell–mediated experimental intestinal inflammations. Therefore, the CAG may be an attractive therapeutic target to specifically suppress the expansion of effector memory CD4+ T cells in intestinal inflammation such as that seen in inflammatory bowel disease.
Published Version: doi:10.1084/jem.20112631
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3526363/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:11708623
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