Exclusion of CD43 from the Immunological Synapse Is Mediated by Phosphorylation-Regulated Relocation of the Cytoskeletal Adaptor Moesin

Delon, Jérôme; Kaibuchi, Kozo; Germain, Ronald N.

doi:10.1016/s1074-7613(01)00231-x

Cited by 256 publications

(254 citation statements)

References 52 publications

(4 reference statements)

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“…Ezrin is present in a phosphorylated form in cells before stimulation through Fas, antigen receptors or chemokine receptors, and is dephosphorylated after these stimulations (Kondo et al, 1997;Delon et al, 2001;Brown et al, 2003;Faure et al, 2004;Gupta et al, 2006;Hao et al, 2009). Our observation that ezrin was dephosphorylated after FasL stimulation in T cells (Figure 1c) is in accordance with those reports.…”

Section: Discussionsupporting

confidence: 92%

“…Activated ezrin and moesin are required for the formation of the distal pole complex (Allenspach et al, 2001) and for the movement of a cytotoxic cell to target cells (Mrass et al, 2008). Alternatively, lymphocyte activation and remolding involves ezrin/moesin inactivation and dissociation from cortical actin (Delon et al, 2001;Brown et al, 2003;Faure et al, 2004;Gupta et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Ezrin is a negative regulator of death receptor-induced apoptosis

et al. 2009

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Ezrin links cortical actin filaments with the cell membrane, and has a critical role in many membrane-initiated events. Fas is directly associated with ezrin, but conflicting results have been reported for the involvement of ezrin in Fas-induced cell death. In this study we show that ezrin was associated with Fas in T cells before stimulation and was released shortly after Fas ligand (FasL) engagement. The knockdown of ezrin moderately increased Fastriggered or tumor necrosis factor-related apoptosisinducing ligand (TRAIL)-triggered cell death in normal T lymphocytes and in H9 cells, but had no effect on death receptor-induced apoptosis in type II cells, such as Jurkat and CEM. Expression of a dominant-negative form of ezrin also led to an increased Fas-induced apoptosis in H9 cells. Ezrin deficiency did not affect the internalization of Fas after Fas ligation. Instead, an enhanced formation of death-inducing signaling complex (DISC) was observed in H9 cells with ezrin knockdown, leading to accelerated caspase-8 activation. Together, our results suggest that ezrin has a negative role in the recruitment of Fas into signaling complexes in type I T cells. Loss of ezrin likely removes the constraint imposed by ezrin and facilitates the assembly of death receptor complex in T cells.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Ezrin is a negative regulator of death receptor-induced apoptosis

et al. 2009

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“…Subsequent studies identified the distal SMAC (dSMAC), an outer region that contains large molecules such as CD43 and CD45 (Delon et al 2001;Freiberg et al 2002). Real time visualization of the early events of T-cell activation has given greater temporal and spatial accuracy.…”

Section: Lat Microclusters: Sites Of Nucleation Of Signaling Complexesmentioning

confidence: 99%

The LAT Story: A Tale of Cooperativity, Coordination, and Choreography

Balagopalan¹,

Coussens²,

Sherman³

et al. 2010

Cold Spring Harbor Perspectives in Biology

152

184

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The adapter molecule LAT is a nucleating site for multiprotein signaling complexes that are vital for the function and differentiation of T cells. Extensive investigation of LAT in multiple experimental systems has led to an integrated understanding of the formation, composition, regulation, dynamic movement, and function of LAT-nucleated signaling complexes. This review discusses interactions of signaling molecules that bind directly or indirectly to LAT and the role of cooperativity in stabilizing LAT-nucleated signaling complexes. In addition, it focuses on how imaging studies visualize signaling assemblies as signaling clusters and demonstrate their dynamic nature and cellular fate. Finally, this review explores the function of LAT based on the interpretation of mouse models using various LAT mutants.

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“…Adhesion molecules have to then hold the two cells together. ERMs have been implicated in all these processes [49,50,51] . Interestingly, a similar array of ERMmediated cytoskeletal rearrangements occurs during infection of lymphocytes by HIV-1.…”

Section: The Immunological Synapse -An Example Of Erm Functional Divementioning

confidence: 99%