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卡波西肉瘤:炎症细胞因子、血管生成因子和病毒因子相互作用的结果。

Kaposi's sarcoma: a result of the interplay among inflammatory cytokines, angiogenic factors and viral agents.

作者信息

Ensoli B, Stürzl M

机构信息

Laboratory of Virology, Istituto Superiore di Sanità, Rome, Italy.

出版信息

Cytokine Growth Factor Rev. 1998 Mar;9(1):63-83. doi: 10.1016/s1359-6101(97)00037-3.

Abstract

Kaposi's sarcoma (KS) is an angioproliferative disease occurring in 4 clinic-epidemiologic forms. Although the AIDS-associated KS (AIDS-KS) is the most aggressive, all forms of KS share the same immunological and histopathological features suggesting common etiological and pathogenic factors. Recent data indicate that at least in early stage KS is not a real sarcoma but an angiohyperplastic-inflammatory lesion mediated by inflammatory cytokines and angiogenic factors, that is triggered or amplified by infection with human herpesvirus-8. In addition, the human immunodeficiency virus type-1 Tat protein appears to be responsible for the higher grade of aggressiveness of AIDS-KS as compared to the other forms of KS. However, given time, reactive KS may progress to a sarcoma as suggested by evidence of monoclonality in late-nodular lesions.

摘要

卡波西肉瘤(KS)是一种血管增殖性疾病,有4种临床流行病学类型。尽管与艾滋病相关的卡波西肉瘤(AIDS-KS)最为侵袭性,但所有类型的KS都具有相同的免疫和组织病理学特征,提示存在共同的病因和致病因素。最近的数据表明,至少在早期,KS并非真正的肉瘤,而是由炎症细胞因子和血管生成因子介导的血管增生性炎症病变,由人类疱疹病毒8型感染引发或放大。此外,与其他类型的KS相比,人类免疫缺陷病毒1型Tat蛋白似乎是AIDS-KS更高侵袭性的原因。然而,随着时间推移,有证据表明晚期结节性病变存在单克隆性,反应性KS可能会进展为肉瘤。

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