Structures of proteinase 3 and the CD177 receptor complex reveal a major autoantibody epitope

Granulomatosis with polyangiitis is a life-threatening systemic vasculitis, characterised by anti-neutrophil cytoplasmic autoantibodies (ANCA) most commonly against proteinase 3 (PR3), a protease expressed intracellularly and on the surface of neutrophils. Most cell surface PR3 is bound to the receptor CD177; however, the molecular mechanism of the interactions is not well understood. Here, we present crystal structures of CD177 in complex with PR3 and unliganded CD177. We describe a mainly hydrophobic binding interface between PR3 and CD177, involving the first two Ly6/uPAR (LU) domains of CD177. These form a globular structure which is connected to downstream domains via a flexible linker. Using a panel of PR3-ANCA-positive patient samples, we show that a significant proportion of ANCAs target the CD177-binding site of PR3 in these samples. Structure-guided mutation of the CD177-binding site on PR3 is effective in reducing PR3-ANCA binding. The results demonstrate that the CD177-binding surface of PR3 harbours a major PR3-ANCA epitope, and that the extent of binding to this surface varies between different patients.

Authors

Institutions

Publication Details

Journal
EMBO Reports
Published
2026-02-17
DOI
https://doi.org/10.1038/s44319-026-00716-5
Primary Topic
Vasculitis and related conditions
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Structures of proteinase 3 and the CD177 receptor complex reveal a major autoantibody epitope

Shirish Dubey, Céline Zheng, E.D. Lowe, S. J. Draper et al.
EMBO Reports
Vasculitis and related conditions
article

Structures of proteinase 3 and the CD177 receptor complex reveal a major autoantibody epitope

Shirish Dubey, Céline Zheng, E.D. Lowe, S. J. Draper, Elena Seiradake, M. Carrasquero, Kirsty McHugh, K. el Omari, Jana Joha, AD Salama, Yu-Chi Chang, Hsi-Hsien Lin
article en

Abstract

Granulomatosis with polyangiitis is a life-threatening systemic vasculitis, characterised by anti-neutrophil cytoplasmic autoantibodies (ANCA) most commonly against proteinase 3 (PR3), a protease expressed intracellularly and on the surface of neutrophils. Most cell surface PR3 is bound to the receptor CD177; however, the molecular mechanism of the interactions is not well understood. Here, we present crystal structures of CD177 in complex with PR3 and unliganded CD177. We describe a mainly hydrophobic binding interface between PR3 and CD177, involving the first two Ly6/uPAR (LU) domains of CD177. These form a globular structure which is connected to downstream domains via a flexible linker. Using a panel of PR3-ANCA-positive patient samples, we show that a significant proportion of ANCAs target the CD177-binding site of PR3 in these samples. Structure-guided mutation of the CD177-binding site on PR3 is effective in reducing PR3-ANCA binding. The results demonstrate that the CD177-binding surface of PR3 harbours a major PR3-ANCA epitope, and that the extent of binding to this surface varies between different patients.

EMBO ReportsVol. 27(6)
Chang Gung University (TW), The Royal Free Hospital (GB), Nuffield Orthopaedic Centre (GB), Diamond Light Source (GB), Chang Gung Memorial Hospital (TW), University of Oxford (GB), Linkou Chang Gung Memorial Hospital (TW), Science Oxford (GB), Oxford University Hospitals NHS Trust (GB), University College London (GB)
Wellcome Trust, Diamond Light Source, Chang Gung Medical Foundation, National Science and Technology Council
Openalex Percentile: Top 54%
Vasculitis and related conditions
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.