| Literature DB >> 27725125 |
Mario A Pulido1, Meleeneh Kazarian DerHartunian1, Zhenxia Qin2, Eric M Chung1, Diane S Kang1, Andrew W Woodham3, Jeffrey A Tsou1, Rinse Klooster1, Omid Akbari3, Lina Wang4, W Martin Kast3, Stephen V Liu5, Jan J G M Verschuuren6, Dana W Aswad2, Ite A Laird-Offringa1.
Abstract
Autoantibodies against SCLC-associated neuronal antigen ELAVL4 (HuD) have been linked to smaller tumors and improved survival, but the antigenic epitope and mechanism of autoimmunity have never been solved. We report that recombinant human ELAVL4 protein incubated under physiological conditions acquires isoaspartylation, a type of immunogenic protein damage. Specifically, the N-terminal region of ELAVL4, previously implicated in SCLC-associated autoimmunity, undergoes isoaspartylation in vitro, is recognized by sera from anti-ELAVL4 positive SCLC patients and is highly immunogenic in subcutaneously injected mice and in vitro stimulated human lymphocytes. Our data suggest that isoaspartylated ELAVL4 is the trigger for the SCLC-associated anti-ELAVL4 autoimmune response.Entities:
Keywords: Autoimmunity; Isoaspartylation; SCLC; Small cell lung cancer
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Year: 2016 PMID： 27725125 PMCID： PMC5152694 DOI： 10.1016/j.jneuroim.2016.09.002
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478