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Abstract Number: 1654

Differential Serum Protein Expression in Groups of Psoriatic Arthritis Patients Characterised By Specific HLA Genotypes and Clinical Features

Musaab Elmamoun1, Angela McArdle2, Muhammad Haroon3, Robert Winchester4, Stephen R. Pennington5 and Oliver FitzGerald6, 1Rheumatology, St. Vincent's University Hospital, Department of Rheumatology, Dublin 4, Ireland, 2University College Dublin, Dublin, Ireland, 3St. Vincent's University Hospital, Department of Rheumatology, Dublin, Ireland, 4Rheumatology, Columbia University, College of Physicians & Surgeons, New York, NY, 5UCD Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin 4, Ireland, 6St. Vincent's University Hospital, Department of Rheumatology. UCD Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin, Ireland

Meeting: 2016 ACR/ARHP Annual Meeting

Date of first publication: September 28, 2016

Keywords: Proteomics and psoriatic arthritis

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Session Information

Date: Monday, November 14, 2016

Title: Spondylarthropathies Psoriatic Arthritis – Pathogenesis, Etiology - Poster I

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose: Psoriatic arthritis (PsA) is a heterogeneous disease with diverse clinical and radiographic manifestations. A number of human leukocyte antigen (HLA) alleles have been found to be associated with PsA.1 HLA-C*06:02 is associated with severe skin disease and a late onset, milder musculoskeletal phenotype; HLA-B*27:05 with entheseal-based disease, severe musculoskeletal disease, enthesitis, symmetric sacroiliitis (SI) and mild psoriasis; HLA-B*08:01 with synovial-based disease, asymmetric SI, joint deformity, joint fusion and dactylitis while HLA-B*38:01/39:01 is associated with more axial involvement and joint damage progression.2 Our hypothesis is that in each of these distinct genetic groups and perhaps as a consequence of the inflammatory events that occur following MHC-peptide interaction, a different pattern of inflammation involving diverse systemic molecules and mediators may be unleashed which in turn determines clinical phenotype and possibly therapeutic response. Our objective is to identify whether there are differences in serum protein expression between groups of patients with specific combinations of HLA genotypes and clinical features.

Methods: Patients with a diagnosis of PsA, fulfilling the CASPAR criteria, aged >18 years were clinically assessed, 10 patients from each of the 4 defined HLA groups. We included a fifth distinct clinical group, Arthritis Mutilans, which as yet has no defined genotype. Serum samples were obtained from all patients. Proteomics Strategy: Serum samples from patients in each of the 5 groups were pooled. Serum pools were depleted of high-abundant proteins. The protein concentration of the remaining low abundant protein fractions was measured and subsequently, protein was digested. Finally, samples were purified prior to liquid chromatography-mass spectrometry LC-MS/MS analysis. Data was imported into MaxQuant and Perseus for quantitative and statistical analysis.

Results: Replicate LC-MS/MS analysis of each the 5 pools (n=3) revealed that a total of 437 proteins could be identified. Of these proteins, 219 were found to be significantly differentially expressed between the different groups (False Discovery Rate: 0.01, p≤ 0.05). Table 1 describes the number of proteins differentially expressed when comparing one PsA subgroup to the other 4 combined groups.

Comparison Univariate Analysis (p value ≤0.05)
Arthritis Mutilans vs. Other Genotypes 43 proteins
B*27 vs. Other Genotypes 28 proteins
B*08 vs. Other Genotypes 91 proteins
B*38/39 vs. Other Genotypes 37 proteins
C*06 vs. Other Genotypes 20 proteins

Table1 shows the discovery data analysis summary

Conclusion: In this study, it was possible to identify proteins that were significantly differentially expressed across the 5 PsA phenotypes. Validation strategies are in progress to measure all differentially expressed proteins in individual patient samples using a targeted proteomics approach. This work is an important first step toward the development of a protein biomarker panel that can be used to distinguish between different PsA subgroups. References: 1. Winchester R, et al. A&R64:1134-44, 2012 2. Haroon M, et al. ARD75:155-162, 2016


Disclosure: M. Elmamoun, None; A. McArdle, None; M. Haroon, None; R. Winchester, None; S. R. Pennington, None; O. FitzGerald, Abbott Immunology Pharmaceuticals, 2,Pfizer Inc, 2,Bristol-Myers Squibb, 2,Abbott Immunology Pharmaceuticals, 5,Pfizer Inc, 5,Bristol-Myers Squibb, 5,Celgene, 5,Janssen Pharmaceutica Product, L.P., 5,Novartis Pharmaceutical Corporation, 5,UCB Pharma, 5,Eli Lilly and Company, 5.

To cite this abstract in AMA style:

Elmamoun M, McArdle A, Haroon M, Winchester R, Pennington SR, FitzGerald O. Differential Serum Protein Expression in Groups of Psoriatic Arthritis Patients Characterised By Specific HLA Genotypes and Clinical Features [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). https://acrabstracts.org/abstract/differential-serum-protein-expression-in-groups-of-psoriatic-arthritis-patients-characterised-by-specific-hla-genotypes-and-clinical-features/. Accessed .
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