T cell response

T 细胞反应
  • DOI:
    文章类型: Case Reports
    癌症的自发消退(SR)是一种罕见但有据可查的生物学现象。然而,机制尚待阐明。我们在此报告了乳腺癌的SR在原发部位和转移性腋窝淋巴结均具有自发诱导的T细胞介导的免疫反应。一名52岁的女性左腋下有肿块,被诊断患有小乳腺癌,腋窝淋巴结转移明显。在术前全身检查中,她被诊断出患有严重的2型糖尿病,用胰岛素治疗,一个月后高血糖恢复正常。然后进行左侧乳腺癌的手术。术后组织病理学检查显示乳腺癌在原发部位和转移性腋窝淋巴结均有SR。免疫组织化学研究显示,雌激素受体阳性,AE1/AE3阳性导管癌完全发生坏死,与淋巴结肿瘤结节中CD3阳性T细胞的广泛浸润有关。此外,原发性导管癌细胞也发生单细胞坏死,乳腺中T细胞浸润,B细胞呈淋巴滤泡样组织。这些特征表明,转移性淋巴结中的肿瘤根除和原发性导管癌的消退可能是由于宿主T细胞对导管癌的反应。据我们所知,这是第一份显示乳腺癌自发消退的报告,可能是由于自发诱导的T细胞反应。
    Spontaneous regression (SR) of cancer is a rare but well-documented biological phenomenon. However, the mechanism remains to be elucidated. We herein report a case of the SR of breast cancer at both the primary site and metastatic axillary lymph node with spontaneously-induced T cell-mediated immunological responses. A 52-year-old female with a lump in the left axilla was diagnosed to have a small breast carcinoma with a distinct axillary lymph node metastasis. During the preoperative systemic examination, she was diagnosed to have severe type 2 diabetes mellitus, was treated with insulin, and the hyperglycemia was normalized after one month. Surgery for left breast cancer was then performed. The postoperative histopathological examination revealed the SR of breast cancer at both the primary site and metastatic axillary lymph node. Immunohistochemical studies revealed that estrogen receptor positive, AE1/AE3-positive ductal carcinoma completely underwent necrosis associated with extensive infiltration of CD3-positive T cells in the tumor nodule in the lymph node. In addition, primary ductal carcinoma cells also underwent single cell necrosis with infiltration of T cells with lymph follicle-like organization of B cells in the mammary gland. The features were suggestive that the tumor eradication in the metastatic lymph node and regression of the primary ductal carcinoma could be due to host T cell response to the ductal carcinoma. As far as we know it is the first report that shows the spontaneous regression of breast cancer, probably due to the spontaneously-induced T cell response.
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