Human leukocyte antigen-ABDR genes in pulmonary adenocarcinoma cell lines.

نویسندگان

  • Bo Deng
  • Ru-Wen Wang
  • Yao-Guang Jiang
  • Yi-Dan Lin
  • Qun-You Tan
  • Jing-Hai Zhou
  • Yun-Ping Zhao
  • Tai-Qian Gong
  • Zheng Ma
چکیده

We read with great interest the article in CHEST (July 2002) by Masakazu et al,1 who observed a haplotype loss of class I human leukocyte antigens (HLAs) in several newly established lung cancer cell lines and identified it as a mechanism of tumor escape from the immunosurveillance system of the host. However, as for the HLA genes of lung cancer cell lines passing for many generations, such as the A549 and Calu-6 cell lines, there have been few reports, and the results have been inconclusive. Rimmelzwaan et al2 reported that the genetic types of HLA-AB in A549 cell line become HLA-A30/ HLA-A25 and HLA-B44/HLA-B18, while Hanagiri et al3 reported that the presentation of HLA-A in the A549 cell line becomes HLA-A30/HLA-A26. We present our results on genetic type HLAABDR in the A549 cell line (CCL-185 in the American Type Culture Collection) and in the Calu-6 cell line (HTB-56 in the American Type Culture Collection) via the polymerase chain reaction-sequence-specific priming method4 as follows: (1) HLA-A30/–, HLA-B44/–, HLA-DR7/HLA-DR53 (A549 cell line); and (2) HLAA01/–, HLA-B08/–, HLA-DR17/DR 52 (Calu-6 cell line). The reason for the different results in the two previously published studies2–3 on the A549 cell line may be the 97.6% homology between HLA-A25 and HLA-A26. However, our study results indicated that there is a haplotype loss of HLA-AB in the A549 cell line. Also, there is a haplotype loss in the Calu-6 cell line. Hence, our results strongly support the fact that there is a haplotype loss of HLA class I genes, not only in these newly established cell lines,1 but also in those cell lines continuing for many generations, which may be one kind of biological action that allows the tumor to escape detection by the immunosurveillance system of the host. The HLA-II gene is present in many kinds of tumor cells, such as lung cancer cells. Intriguingly, in spite of continuing for many generations, the two cell lines wholly retain the HLA-DR genes. The result is different from a reported study5 in which there was also found to be a haplotype loss of HLA class II genes in all of the three newly established lung cancer cell lines. The correlative mechanisms of “haplotype loss” and “whole retention” of HLA class I/II genes are novel, and it is necessary to determine their cause as the next step in research.

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عنوان ژورنال:
  • Chest

دوره 134 4  شماره 

صفحات  -

تاریخ انتشار 2008