Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a disease of unknown etiology, manifesting chronic systemic inflammation and resulting in the destruction of joints. As with any inflammatory disease, cytokines and chemokines play an important role in RA’s progression and potentially allow for its monitoring. IL-1 and TNF-α are well known cytokines involved in joint inflammation1.

IL-17 is responsible for monocyte infiltration into the synovium and is a novel RA therapeutic target2. Levels of TNF-RI and TNF-RII have been observed to be higher in patients with rheumatoid arthritis than in healthy individuals3. RANTES, GRO-α, and MCP-1 are all elevated in patients with RA, and the levels of those chemokines drop in response to methotrexate therapy4.

IL-6 and IL-8 are well-known contributors to joint damage and systemic inflammation5, and high levels of eotaxin are inversely associated with radiographic progression of RA6. Matrix metalloproteinase (MMP)-1 and MMP-3, also known as collagenase-1 and stromelysin-1, have been shown to be elevated in the serum of RA patients when compared to healthy controls; they have also been shown to contribute to tissue degradation in the synovium7.

Tissue inhibitor of matrix metalloproteinases (TIMP-1) has long been studied along with MMP-1 in RA with recent research showing that SNPs in the TIMP-1 gene are associated with a higher risk of developing RA8. The flexibility of Quansys’ Build Your Own array allows you to use the above markers or include others in your research of RA.


Serum Markers

IL-1α, IL-1β, TNF-α, IL-17, RANTES (CCL5), GRO-α (CXCL-1), MCP-1 (CCL-2), IL-6, MMP-1, MMP-3, TIMP-1, TNF-RI, TNF-RII, IL-8, IP-10 (CXCL-10), GMCSF , CRP, and Eotaxin (CCL11)


Rheumatoid Arthritis Markers in Q-Plex™ Kits


  1. Lubberts E, van den Berg WB: Cytokines in the pathogenesis of rheumatoid arthritis and collagen-induced arthritis. Adv Exp Med Biol 2003, 520:194-202
  2. Shahrara S, Pickens SR, Dorfleutner A, Pope RM: IL-17 induces monocyte migration in rheumatoid arthritis. J Immunol 2009, 182:3884-3891.
  3. Valle Y, Ledezma-Lozano IY, Torres-Carrillo N, Padilla-Gutierrez JR, Navarro-Hernandez RE, Vazquez-Del Mercado M, Palafox-Sanchez CA, Armendariz-Borunda J, Munoz-Valle JF: Circulating TNFRI and TNFRII levels correlated with the disease activity score (DAS28) in rheumatoid arthritis. Scand J Rheumatol 2009, 38:332-335.
  4. Boiardi L, Macchioni P, Meliconi R, Pulsatelli L, Facchini A, Salvarani C: Relationship between serum RANTES levels and radiological progression in rheumatoid arthritis patients treated with methotrexate. Clin Exp Rheumatol 1999, 17:419-425.
  5. Georganas C, Liu H, Perlman H, Hoffmann A, Thimmapaya B, Pope RM: Regulation of IL-6 and IL-8 expression in rheumatoid arthritis synovial fibroblasts: the dominant role for NF-kappa B but not C/EBP beta or c-Jun. J Immunol 2000, 165:7199-7206.
  6. Syversen SW, Goll GL, Haavardsholm EA, Boyesen P, Lea T, Kvien TK: A high serum level of eotaxin (CCL 11) is associated with less radiographic progression in early rheumatoid arthritis patients. Arthritis Res Ther 2008, 10:R28.
  7. Green MJ, Gough AK, Devlin J, Smith J, Astin P, Taylor D, Emery P: Serum MMP-3 and MMP-1 and progression of joint damage in early rheumatoid arthritis. Rheumatology (Oxford) 2003, 42:83-88.
  8. Burkhardt J, Petit-Teixeira E, Teixeira VH, Kirsten H, Garnier S, Ruehle S, Oeser C, Wolfram G, Scholz M, Migliorini P, et al: Association of the X-chromosomal genes TIMP1 and IL9R with rheumatoid arthritis. J Rheumatol 2009, 36:2149-2157.

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