Weyand C M, Hicok K C, Hunder G G, Goronzy J J
Mayo Clinic, Rochester, Minnesota.
Ann Intern Med. 1994 Oct 1;121(7):484-91. doi: 10.7326/0003-4819-121-7-199410010-00003.
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.
Case series of patients having temporal artery biopsy procedures.
The outpatient clinic and the research laboratories of the Division of Rheumatology, Mayo Clinic.
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.
Temporal artery specimens were analyzed for in vivo presence of cytokine messenger RNA (mRNA) by polymerase chain reaction with cytokine-specific primer sets.
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.
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.
分析巨细胞动脉炎和风湿性多肌痛患者的颞动脉标本中炎性细胞因子的存在情况，并确定这两种疾病是否存在特定的细胞因子模式。
对接受颞动脉活检的患者进行病例系列研究。
梅奥诊所风湿病科门诊及研究实验室。
34例接受颞动脉活检的患者：15例患有巨细胞动脉炎，9例患有无血管炎证据的风湿性多肌痛，10例既无风湿性多肌痛也无血管炎。
通过使用细胞因子特异性引物对的聚合酶链反应分析颞动脉标本中细胞因子信使核糖核酸（mRNA）的体内存在情况。
巨细胞动脉炎样本中的血管病变特征为白细胞介素-1β、白细胞介素-6和转化生长因子-β1 mRNA的原位产生（表明巨噬细胞活化）以及干扰素-γ和白细胞介素-2 mRNA的原位产生（表明选择性T细胞活化）。然而，在风湿性多肌痛患者的颞动脉活检标本中也检测到了巨噬细胞和T细胞衍生的细胞因子。巨细胞动脉炎和风湿性多肌痛样本中的组织浸润性T细胞各自具有独特的淋巴因子谱。虽然在67%的巨细胞动脉炎样本中发现了干扰素-γ，但风湿性多肌痛样本中只有白细胞介素-2。
风湿性多肌痛患者存在血管受累。风湿性多肌痛和巨细胞动脉炎患者共享巨噬细胞衍生细胞因子特异性mRNA的原位产生。招募到巨细胞动脉炎患者血管病变中的T细胞主要产生白细胞介素-
