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Impaired activation and localization of LAT in anergic T cells as a consequence of a selective palmitoylation defect.

Abstract：

:The molecular basis of T cell anergy is not completely understood. We show that in antigen-primed anergic murine CD4(+) T cells the linker for activation of T cells (LAT) is hypophosphorylated upon CD3/CD28 restimulation. Signaling events downstream of LAT (PLCgamma1 phosphorylation and p85 [PI3-K] association) were impaired, whereas upstream events (CD3zeta and ZAP-70 phosphorylation) remained intact. LAT recruitment to the immunological synapse and its localization in detergent-resistant membrane (DRM) fractions were defective in anergic T cells. These defects resulted from impaired palmitoylation of LAT and were selective since the DRM localization and palmitoylation of Fyn were intact. This LAT defect was independent of Cbl-b and did not reflect enhanced LAT degradation. These results identify LAT as the most upstream target of anergy induction; moreover, they suggest that regulation of the amount of LAT in the immunological synapse and DRM by posttranslational palmitoylation contributes to the induction of T cell anergy.

journal_name

Immunity

journal_title

Immunity

authors

Hundt M,Tabata H,Jeon MS,Hayashi K,Tanaka Y,Krishna R,De Giorgio L,Liu YC,Fukata M,Altman A

doi

10.1016/j.immuni.2006.03.011

subject

Has Abstract

pub_date

2006-05-01 00:00:00

pages

513-22

issue

5

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(06)00209-3

journal_volume

24

pub_type

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