B Cell Antigen Receptor Signal Strength and Peripheral B Cell Development are Regulated by a 9-O-Acetyl Sialic Acid Esterase

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B Cell Antigen Receptor Signal Strength and Peripheral B Cell Development are Regulated by a 9-O-Acetyl Sialic Acid Esterase

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Title: B Cell Antigen Receptor Signal Strength and Peripheral B Cell Development are Regulated by a 9-O-Acetyl Sialic Acid Esterase
Author: Cariappa, Annaiah; Takematsu, Hiromu; Liu, Haoyuan; Diaz, Sandra; Haider, Khaleda; Kalloo, Geetika; Varki, Nissi; Varki, Ajit; Boboila, Cristian; Connole, Michelle Ann; Shi, Hai Ning; Pillai, Shiv Subramaniam

Note: Order does not necessarily reflect citation order of authors.

Citation: Cariappa, Annaiah, Hiromu Takematsu, Haoyuan Liu, Sandra Diaz, Khaleda Haider, Cristian Boboila, Geetika Kalloo, et al. 2009. B cell antigen receptor signal strength and peripheral B cell development are regulated by a 9-O-acetyl sialic acid esterase. Journal of Experimental Medicine 206(1): 125-138.
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Abstract: We show that the enzymatic acetylation and deacetylation of a cell surface carbohydrate controls B cell development, signaling, and immunological tolerance. Mice with a mutation in sialate:O-acetyl esterase, an enzyme that specifically removes acetyl moieties from the 9-OH position of α2–6-linked sialic acid, exhibit enhanced B cell receptor (BCR) activation, defects in peripheral B cell development, and spontaneously develop antichromatin autoantibodies and glomerular immune complex deposits. The 9-O-acetylation state of sialic acid regulates the function of CD22, a Siglec that functions in vivo as an inhibitor of BCR signaling. These results describe a novel catalytic regulator of B cell signaling and underscore the crucial role of inhibitory signaling in the maintenance of immunological tolerance in the B lineage.
Published Version: doi:10.1084/jem.20081399
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626685/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:4853404

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