Orientation-dependent CD45 inhibition with viral and engineered ligands

CD45 is a cell surface phosphatase that shapes the T cell receptor signaling threshold but does not have a known ligand. A family of adenovirus proteins, including E3/49K, exploits CD45 to evade immunity by binding to the extracellular domain of CD45, resulting in the suppression of T cell signaling. We determined the cryo-EM structure of this complex and found that the E3/49K protein is composed of three immunoglobulin domains assembled as "beads on a string" that compel CD45 into a closely abutted dimer by cross-linking the CD45 D3 domain, leading to steric inhibition of its intracellular phosphatase activity. Inspired by the E3/49K mechanism, we engineered CD45 surrogate ligands that can fine-tune T cell activation by dimerizing CD45 into different orientations and proximities. The adenovirus E3/49K protein has taught us that, despite a lack of a known ligand, CD45 activity can be modulated by extracellular dimerizing ligands that perturb its phosphatase activity and alter T cell responses.

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Publication Details

Journal
Science Immunology
Published
2024-10-25
DOI
https://doi.org/10.1126/sciimmunol.adp0707
Citations
4
Primary Topic
Immune Cell Function and Interaction
Type
article
Field-Weighted Citation Impact
0.96

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Orientation-dependent CD45 inhibition with viral and engineered ligands

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4 citations
Science Immunology
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article

Orientation-dependent CD45 inhibition with viral and engineered ligands

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article en
4 citations

Abstract

CD45 is a cell surface phosphatase that shapes the T cell receptor signaling threshold but does not have a known ligand. A family of adenovirus proteins, including E3/49K, exploits CD45 to evade immunity by binding to the extracellular domain of CD45, resulting in the suppression of T cell signaling. We determined the cryo-EM structure of this complex and found that the E3/49K protein is composed of three immunoglobulin domains assembled as "beads on a string" that compel CD45 into a closely abutted dimer by cross-linking the CD45 D3 domain, leading to steric inhibition of its intracellular phosphatase activity. Inspired by the E3/49K mechanism, we engineered CD45 surrogate ligands that can fine-tune T cell activation by dimerizing CD45 into different orientations and proximities. The adenovirus E3/49K protein has taught us that, despite a lack of a known ligand, CD45 activity can be modulated by extracellular dimerizing ligands that perturb its phosphatase activity and alter T cell responses.

Science ImmunologyVol. 9(100)
Howard Hughes Medical Institute (US), Harvard University (US), University of California San Diego (US), Dana-Farber Cancer Institute (US), Stanford University (US)
Howard Hughes Medical Institute, Ludwig Institute for Cancer Research, National Institutes of Health, University of California, San Francisco, National Cancer Institute
Openalex Percentile: Top 24%
Immune Cell Function and Interaction
0.96
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