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Tissue Cytokine Patterns in Patients with Polymyalgia Rheumatica and Giant Cell Arteritis

Cornelia M. Weyand, MD, PhD; Kevin C. Hicok, MS; Gene G. Hunder, MD; and Jorg J. Goronzy, MD, PhD
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From the Mayo Clinic, Rochester, Minnesota. Requests for Reprints: Cornelia M. Weyand, MD, PhD, Mayo Clinic, 401 Guggenheim Building, 200 First Street Southwest, Rochester, MN 55905. Acknowledgments: The authors thank Toni L. Buss for secretarial assistance; Dr. W. O'Fallon for statistical advice; and their colleagues for their help in studying their patients. Grant Support: In part by a grant-in-aid from the American Heart Association and by the Mayo Foundation. Dr. Weyand is the recipient of an Arthritis Foundation Investigator Award.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1994;121(7):484-491. doi:10.7326/0003-4819-121-7-199410010-00003
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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 β, interleukin-6, and transforming growth factor-β 1 mRNA (indicative of macrophage activation) and by interferon-γ 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-γ 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-γ. Patients with polymyalgia rheumatica do not have interferon-γ production, suggesting that interferon-γ may be involved in the progression to overt arteritis.


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Figure 1.
Macrophage-derived cytokine mRNA in temporal artery specimens using polymerase chain reaction.

Lanes 2 to 6 represent specimens from patients with giant cell arteritis; lanes 7 to 9 represent control patients. Lane 1 represents a positive control. GM-CSF = granulocyte–macrophage-colony stimulating factor; IL = interleukin; mRNA = messenger RNA; S = size marker; TGF = transforming growth factor; TNF = tumor necrosis factor.

Grahic Jump Location
Grahic Jump Location
Figure 2.
Polymerase chain reaction amplification of lymphokine-specific sequences.

Lanes 2 to 6 represent specimens from patients with giant cell arteritis; lanes 7 to 9 represent control patients. Lane 1 represents a positive control. IFN = interferon; IL = interleukin; S = size marker; TCR = T-cell receptor.

Grahic Jump Location




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