期刊
PLOS ONE
卷 6, 期 5, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0019911
关键词
-
资金
- Japan Science and Technology Agency
- Ministry of Education, Culture, Sports, Science and Technology [20390448, 20390087, 20592075, 20791678]
- Takeda Science Foundation
- Uehara Memorial Foundation
- Naito Foundation
- Novartis Foundation [20-10]
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Senri Life Science Foundation [S-2144]
- Kato Memorial Bioscience Foundation
- Japan National Society for the Prevention of Blindness
- National Institute of Health [E13053]
- Grants-in-Aid for Scientific Research [23592603, 20592075, 20390448, 20791678, 23592561, 20390087, 23390074] Funding Source: KAKEN
Background: Paraneoplastic retinopathy (PR), including cancer-associated retinopathy (CAR) and melanoma-associated retinopathy (MAR), is a progressive retinal disease caused by antibodies generated against neoplasms not associated with the eye. While several autoantibodies against retinal antigens have been identified, there has been no known autoantibody reacting specifically against bipolar cell antigens in the sera of patients with PR. We previously reported that the transient receptor potential cation channel, subfamily M, member 1 (TRPM1) is specifically expressed in retinal ON bipolar cells and functions as a component of ON bipolar cell transduction channels. In addition, this and other groups have reported that human TRPM1 mutations are associated with the complete form of congenital stationary night blindness. The purpose of the current study is to investigate whether there are autoantibodies against TRPM1 in the sera of PR patients exhibiting ON bipolar cell dysfunction. Methodology/Principal Findings: We performed Western blot analysis to identify an autoantibody against TRPM1 in the serum of a patient with lung CAR. The electroretinograms of this patient showed a severely reduced ON response with normal OFF response, indicating that the defect is in the signal transmission between photoreceptors and ON bipolar cells. We also investigated the sera of 26 patients with MAR for autoantibodies against TRPM1 because MAR patients are known to exhibit retinal ON bipolar cell dysfunction. Two of the patients were found to have autoantibodies against TRPM1 in their sera. Conclusion/Significance: Our study reveals TRPM1 to be one of the autoantigens targeted by autoantibodies in at least some patients with CAR or MAR associated with retinal ON bipolar cell dysfunction.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据