TISSUE CYTOKINE PATTERNS IN PATIENTS WITH POLYMYALGIA-RHEUMATICA AND GIANT-CELL ARTERITIS

Objective: To analyze temporal artery specimens from patients with giant cell arteritis and polymyalgia rheumatica for the presence of inflammatory cytokines and to ascertain whether a specific cytokine pattern exists for the two conditions. Design: Case series of patients having temporal artery biopsy procedures. Setting: The outpatient clinic and the research laboratories of the Division of Rheumatology, Mayo Clinic. Patients: 34 patients having temporal artery biopsy procedures: 15 patients had giant cell arteritis, 9 had polymyalgia rheumatica without evidence of vasculitis, and 10 had neither polymyalgia rheumatica nor vasculitis. Measurement: Temporal artery specimens were analyzed for in vivo presence of cytokine messenger RNA (mRNA) by polymerase chain reaction with cytokine-specific primer sets. Results: Vasculitic lesions in giant cell arteritis samples were characterized by in situ production of interleukin-1 beta, interleukin-6, and transforming growth factor-beta 1 mRNA (indicative of macrophage activation) and by interferon-gamma and interleukin-2 mRNA (indicative of selective T-cell activation). However, macrophage- and T-cell-derived cytokines were also detected in temporal artery biopsy specimens from patients with polymyalgia rheumatica. Tissue-infiltrating T cells in giant cell arteritis and polymyalgia rheumatica samples each had distinctive lymphokine profiles. Although interferon-gamma was found in 67% of giant cell arteritis samples, polymyalgia rheumatica samples had only interleukin-2. Conclusions: Patients with polymyalgia rheumatica have vascular involvement. Patients with polymyalgia rheumatica and giant cell arteritis share in situ production of mRNA specific for macrophage-derived cytokines. T cells recruited to vasculitic lesions in patients with giant cell arteritis predominantly produce interleukin-2 and interferon-gamma. Patients with polymyalgia rheumatica do not have interferon-gamma production, suggesting that interferon-gamma may be involved in the progression to overt arteritis.