HTLV-I virological and histopathological analysis in two cases of anti-centromere-antibody-seropositive Sjogren's syndrome
HTLV-I virological and histopathological analysis in two cases of anti-centromere-antibody-seropositive Sjogren's syndrome
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DOI：
10.1007/s10165-012-0641-x
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发表时间：
2013-01-01
影响因子：
2.2
通讯作者：
Kawakami, Atsushi
中科院分区：
文献类型：
--
作者：
Nakamura, Hideki;Horai, Yoshiro;Kawakami, Atsushi
本研究旨在探讨抗着丝粒抗体(ACA)阳性干燥综合征(SS)患者的临床和病理特点。记录包括血清HTLV-I滴度、病毒载量和细胞因子谱在内的背景数据。对HAM患者的嘴唇唾液腺(LSG)和肌肉活检标本进行了苯胺蓝(Azan)-Mallory染色和免疫组织化学染色。与HTLV-I携带者相比，HAM-SS患者的血清转化生长因子-β(TGF-β)、肿瘤坏死因子-α(TNF-α)和HTLV-I病毒载量均较高。HAM-SS患者LSG纤维性改变显著。在HAM-SS患者中，HAM-SS患者LSG中主要表达HTLV-I相关蛋白，包括p12、p28、组特异性抗原(GAG)和核因子-kappaB(NF-kappa B)。HTLV-I阳性SS伴ACA患者、HTLV-I阴性SS伴ACA患者和HTLV-I阴性SS患者的转化生长因子-β染色频率低于前两组患者。原位高HTLV-I病毒载量可能促进细胞因子尤其是转化生长因子-β的产生，导致ACA阳性SS患者LSG的纤维性改变。
The aim of this study was to show the clinical and pathological characteristics of anti-centromere-antibody (ACA)-seropositive Sjogren's syndrome (SS) in two anti-human T-cell leukemia virus type I (HTLV-I)-seropositive patients.One patient was an HTLV-I carrier whereas the other was diagnosed with HTLV-I-associated myelopathy (HAM). Background data including serum HTLV-I titers, viral loads, and cytokine profiles were recorded. Azocarmine with aniline blue (Azan)-Mallory staining and immunohistochemistry of the labial salivary glands (LSGs) and a muscle biopsy specimen from the HAM patient were performed.Serum transforming growth factor beta (TGF-beta), tumor necrosis factor alpha (TNF-alpha), and HTLV-I viral load were high in the HAM-SS patient compared with the HTLV-I carrier. Fibrous change in LSG was prominent in the HAM-SS patient. Although TGF-beta expression was similar in the two patients, expression of HTLV-I-related proteins including p12, p28, group-specific antigen (GAG), and nuclear factor kappa-B (NF-kappa B) in the LSG were dominantly detected in the HAM-SS patient. Frequency of TGF-beta staining in HTLV-I-seropositive SS patients without ACA, HTLV-I-seronegative SS patients with ACA, and HTLV-I-seronegative SS patients without ACA was lower than that of the previous two patients.A high HTLV-I viral load in situ is supposed to promote the production of cytokines, especially TGF-beta, resulting in the fibrous change of LSG in ACA-seropositive SS patients.