Saturday, October 10, 2009

TCE induced auto immunity

BrooklynDodger(s) Comments: Reading this abstract, the Dodger(s) discovered an apparently well accepted association between TCE exposure and exfoliative dermatitis, as Type II cell mediated auto immune condition. Waving hands, the Dodger(s) imagine TCE induced cell necrosis, possibly liver, triggering lymphocyte attack on debris, growing a clone of lymphocytes targeting cell surface proteins of a variety of tissues.

Toxicology and Applied Pharmacology
Volume 240, Issue 3, 1 November 2009, Pages 393-400
Identification of antigenic proteins associated with trichloroethylene-induced autoimmune disease by serological proteome analysis

Jianjun Liu1, a, Xiumei Xing1, a, Haiyan Huanga, Yingzhi Jianga, Haowei Hea, Xinyun Xua, Jianhui Yuana, Li Zhoua, Linqing Yanga and Zhixiong ZhuangCorresponding Author Contact Information, a, E-mail The Corresponding Author

aKey Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, No. 21, Rd 1st Tianbei, 518020 Shenzhen, PR China

Received 1 April 2009;
revised 8 July 2009;
accepted 25 July 2009.
Available online 6 August 2009.


Although many studies indicated that trichloroethylene (TCE) could induce autoimmune diseases and some protein adducts were detected, the proteins were not identified and mechanisms remain unknown. To screen and identify autoantigens which might be involved in TCE-induced autoimmune diseases, three groups of sera were collected from healthy donors (I), patients suffering from TCE-induced exfoliative dermatitis (ED) (II), and the healed ones (III). Serological proteome analysis (SERPA) was performed with total proteins of TCE-treated L-02 liver cells as antigen sources and immunoglobins of the above sera as probes. Highly immunogenic spots (2-fold or above increase compared with group I) in group II and III were submitted to matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS) and tandem mass spectrometry sequencing. Western blot analysis was followed using commercial antibodies and individual serum. Six proteins were identified. Among them, Enoyl Coenzyme A hydratase peroxisoma 1 and lactate dehydrogenase B only showed stronger immunogenicity for group II sera, while Purine nucleoside phosphorylase, ribosomal protein P0 and proteasome activator subunit1 isoform1 also showed stronger immunogenicity for group III sera. Noteworthy, NM23 reacted only with group II sera. Western blot analysis of NM23 expression indicated that all of the individual serum of group II showed immune activity, which confirmed the validity of SERPA result. These findings revealed that there exist autoantibodies in group II and III sera. Besides, autoantibodies of the two stages of disease course were different. These autoantigens might serve as biomarkers to elucidate mechanisms underlying TCE toxicity and are helpful for diagnosis, therapy and prognosis of TCE-induced autoimmune diseases.

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