Molecular Medicine

, Volume 11, Issue 1–12, pp 21–29 | Cite as

Microarray Analyses of Peripheral Blood Cells Identifies Unique Gene Expression Signature in Psoriatic Arthritis

  • Franak M. Batliwalla
  • Wentian Li
  • Christopher T. Ritchlin
  • Xiangli Xiao
  • Max Brenner
  • Teresina Laragione
  • Tianmeng Shao
  • Robert Durham
  • Sunil Kemshetti
  • Edward Schwarz
  • Rodney Coe
  • Marlena Kern
  • Emily C. Baechler
  • Timothy W. Behrens
  • Peter K. Gregersen
  • Pércio S. Gulko


Psoriatic arthritis (PsA) is a chronic and erosive form of arthritis of unknown cause. We aimed to characterize the PsA phenotype using gene expression profiling and comparing it with healthy control subjects and patients rheumatoid arthritis (RA). Peripheral blood cells (PBCs) of 19 patients with active PsA and 19 age- and sex-matched control subjects were used in the analyses of PsA, with blood samples collected in PaxGene tubes. A significant alteration in the pattern of expression of 313 genes was noted in the PBCs of PsA patients on Affymetrix U133A arrays: 257 genes were expressed at reduced levels in PsA, and 56 genes were expressed at increased levels, compared with controls. Downregulated genes tended to cluster to certain chromosomal regions, including those containing the psoriasis susceptibility loci PSORS1 and PSORS2. Among the genes with the most significantly reduced expression were those involved in downregulation or suppression of innate and acquired immune responses, such as SIGIRR, STAT3, SHP1, IKBKB, IL-11RA, and TCF7, suggesting inappropriate control that favors proinflammatory responses. Several members of the MAPK signaling pathway and tumor suppressor genes showed reduced expression. Three proinflammatory genes—S100A8, S100A12, and thioredoxin—showed increased expression. Logistic regression and recursive partitioning analysis determined that one gene, nucleoporin 62 kDa, could correctly classify all controls and 94.7% of the PsA patients. Using a dataset of 48 RA samples for comparison, the combination of two genes, MAP3K3 followed by CACNA1S, was enough to correctly classify all RA and PsA patients. Thus, PBC gene expression profiling identified a gene expression signature that differentiated PsA from RA, and PsA from controls. Several novel genes were differentially expressed in PsA and may prove to be diagnostic biomarkers or serve as new targets for the development of therapies.



This work was supported by the National Institutes of Health Autoimmune Biomarkers Collaborative Network contract NO1-AR-1-2256.

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Copyright information

© Feinstein Institute for Medical Research 2005

Authors and Affiliations

  • Franak M. Batliwalla
    • 1
    • 6
  • Wentian Li
    • 1
  • Christopher T. Ritchlin
    • 2
  • Xiangli Xiao
    • 1
  • Max Brenner
    • 1
    • 3
  • Teresina Laragione
    • 1
  • Tianmeng Shao
    • 2
  • Robert Durham
    • 2
  • Sunil Kemshetti
    • 2
  • Edward Schwarz
    • 2
  • Rodney Coe
    • 1
  • Marlena Kern
    • 1
  • Emily C. Baechler
    • 4
  • Timothy W. Behrens
    • 4
  • Peter K. Gregersen
    • 1
    • 5
    • 6
  • Pércio S. Gulko
    • 1
    • 5
    • 6
  1. 1.Robert S. Boas Center for Genomics and Human GeneticsFeinstein Institute for Medical ResearchManhassetUSA
  2. 2.Division of Rheumatology, Department of MedicineUniversity of RochesterRochesterUSA
  3. 3.North Shore-LIJ Graduate School of Molecular MedicineManhassetUSA
  4. 4.Division of Rheumatic and Autoimmune Diseases, Department of MedicineUniversity of MinnesotaMinneapolisUSA
  5. 5.Division of Rheumatology, Department of MedicineNorth Shore University HospitalManhassetUSA
  6. 6.Department of MedicineNew York University School of MedicineNew YorkUSA

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