0
Correspondence |

Human Leukocyte Antigen-ABDR Genes in Pulmonary Adenocarcinoma Cell Lines FREE TO VIEW

Bo Deng, MD; Ru-Wen Wang, MD; Yao-Guang Jiang, MD; Yi-Dan Lin, MD; Qun-You Tan, MD; Jing-Hai Zhou, MD; Yun-Ping Zhao, MD; Tai-Qian Gong, MD; Zheng Ma, MD
Author and Funding Information

Daping Hospital Third Military Medical University Chongqing, People's Republic of China

Correspondence to: Ru-Wen Wang, MD, Thoracic Surgery Department, Daping Hospital Third Military Medical University, Changjiang Branch St, 10, Yuzhong District, Chongqing City, 400042 People's Republic of China; e-mail: superdb@163.com


The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(4):890. doi:10.1378/chest.08-1058
Text Size: A A A
Published online

To the Editor:

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 HLA-ABDR 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) HLA-A01/–, HLA-B08/–, HLA-DR17/DR 52 (Calu-6 cell line).

The reason for the different results in the two previously published studies23 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.

Masakazu S, Mitsuhiro T, Toshihiro O. Establishment of 15 cancer cell lines from patients with lung cancer and the potential tools for immunotherapy. Chest. 2002;122:282-288. [PubMed] [CrossRef]
 
Rimmelzwaan GF, Boon AC, Geelhoed-Mieras MM, et al. Human airway epithelial cells present antigen to influenza virus-specific CD8+ CTL inefficiently after incubation with viral protein together with ISCOMATRIX. Vaccine. 2004;22:2769-2775. [PubMed]
 
Hanagiri T, Yoshino I, Takenoyama M, et al. Effects of interleukin-12 on the induction of cytotoxic T lymphocytes from the regional lymph node lymphocytes of patients with lung adenocarcinoma. Jpn J Cancer Res. 1998;89:192-198. [PubMed]
 
Moribe T, Kaneshige T, Inoko H. Complete HLA-A DNA typing using the PCR-RFLP method combined with allele group- and sequence-specific amplification. Tissue Antigens. 1997;50:535-545. [PubMed]
 
Koopman LA, Corver WE, van der Slik AR, et al. Multiple genetic alterations cause frequent and heterogeneous human histocompatibility leukocyte antigen class I loss in cervical cancer. J Exp Med. 2000;191:961-975. [PubMed]
 

Figures

Tables

References

Masakazu S, Mitsuhiro T, Toshihiro O. Establishment of 15 cancer cell lines from patients with lung cancer and the potential tools for immunotherapy. Chest. 2002;122:282-288. [PubMed] [CrossRef]
 
Rimmelzwaan GF, Boon AC, Geelhoed-Mieras MM, et al. Human airway epithelial cells present antigen to influenza virus-specific CD8+ CTL inefficiently after incubation with viral protein together with ISCOMATRIX. Vaccine. 2004;22:2769-2775. [PubMed]
 
Hanagiri T, Yoshino I, Takenoyama M, et al. Effects of interleukin-12 on the induction of cytotoxic T lymphocytes from the regional lymph node lymphocytes of patients with lung adenocarcinoma. Jpn J Cancer Res. 1998;89:192-198. [PubMed]
 
Moribe T, Kaneshige T, Inoko H. Complete HLA-A DNA typing using the PCR-RFLP method combined with allele group- and sequence-specific amplification. Tissue Antigens. 1997;50:535-545. [PubMed]
 
Koopman LA, Corver WE, van der Slik AR, et al. Multiple genetic alterations cause frequent and heterogeneous human histocompatibility leukocyte antigen class I loss in cervical cancer. J Exp Med. 2000;191:961-975. [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543