Anti-melanoma cytotoxic T lymphocytes (CTL) recognize numerous antigenic peptides having 'self' sequences: autoimmune nature of the anti-melanoma CTL response.
Anti-melanoma cytotoxic T lymphocytes (CTL) recognize numerous antigenic peptides having 'self' sequences: autoimmune nature of the anti-melanoma CTL response.
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抗黑色素瘤细胞毒性 T 淋巴细胞 (CTL) 识别许多具有“自身”序列的抗原肽：抗黑色素瘤 CTL 反应的自身免疫性质。
DOI：
10.1093/intimm/9.2.327
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发表时间：
1997
影响因子：
4.4
通讯作者：
Eisen,HN
中科院分区：
文献类型：
--
作者：
Tsomides,TJ;Reilly,EB;Eisen,HN
肿瘤浸润淋巴细胞系（660 TIL）特异性裂解自体HLA-A2+黑素瘤（660 MEL）和大多数A2+黑素瘤细胞系。我们从大量（>10（12））的660 MEL细胞中免疫沉淀A2，提取天然加工的肽，通过HPLC将其分级，筛选660 TIL识别的级分，并发现单一的主要活性峰和次要活性峰。虽然回收的主要660 MEL肽太少而无法确定其序列，但HPLC指纹图谱显示其不对应于任何已知的由T细胞识别的A2相关黑素瘤肽，包括来自酪氨酸酶、MART-1/Melan-A、gp 100和法师-3的肽。主要的660 MEL抗原肽似乎来源于MART-1/Melan-A，但既不是AAGIGILTV，也不是ILTVILGVL，也不是任何其他含有A2共有基序的MART-1/Melan-A肽。由CD 8 + T细胞识别的黑色素瘤肽的多样性，其中大多数是非突变的（包括最有可能存在的660 MEL肽），表明存在未知的机制，可能类似于在自身免疫性疾病中的那些机制，从而识别正常“自身”序列的T细胞被激活。
A line of tumor-infiltrating lymphocytes (660TIL) specifically lysed the autologous HLA-A2+ melanoma (660MEL) and also most A2+ melanoma cell lines. We immunoprecipitated A2 from a large number (>10(12)) of 660MEL cells, extracted naturally processed peptides, fractionated them by HPLC, screened the fractions for recognition by 660TIL, and found a single predominant and a minor peak of activity. Although too little was recovered of the major 660MEL peptide to establish its sequence, HPLC fingerprinting showed that it did not correspond to any of the known A2-associated melanoma peptides recognized by T cells, including peptides from tyrosinase, MART-1/Melan-A, gp100 and MAGE-3. The major 660MEL antigenic peptide appears to be derived from MART-1/Melan-A but is neither AAGIGILTV nor ILTVILGVL nor any other MART-1/Melan-A peptide containing the A2 consensus motif. The multiplicity of melanoma peptides recognized by CD8+ T cells, most of which are non-mutated (including most likely the present 660MEL peptide), suggests the existence of unknown mechanisms, perhaps similar to those operating in autoimmune disorders, whereby T cells that recognize normal 'self' sequences become activated.