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.