期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 206, 期 1, 页码 125-138出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20081399
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资金
- NHLBI NIH HHS [P01 HL057345, P01HL057345] Funding Source: Medline
- NIAID NIH HHS [AI069458, R21 AI069458, R01 AI064930, AI064930] Funding Source: Medline
- NIDDK NIH HHS [P30 DK043351] Funding Source: Medline
- NIGMS NIH HHS [R01 GM032373, R37 GM032373, GM32373] Funding Source: Medline
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 alpha 2-6-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.
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