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. 2015 Sep 30;11(9):e1005183. doi: 10.1371/journal.ppat.1005183

Fig 7. HCV E2 protein inhibits distal T cell receptor (TCR) signaling.

Fig 7

PMA + Ionomycin (P+I) mediated IL-2 release by Jurkat cells expressing full-length or various truncated or tyrosine 613 mutant HCV E2 protein fragments as indicated (A). Recombinant HCV E2 protein was phosphorylated by Lck in an in vitro kinase reaction, and was dephosphorylated by the CD45 phosphatase (B). HCV E2 protein (native, or Y613A mutant) expressed in Jurkat cells was precipitated before (-) or after (+) TCR stimulation with anti-CD3. E2 and phospho-E2 were detected by immunoblot with E2 specific antibody or anti-phosphotyrosine antibody respectively (C). P+I mediated IL-2 release control Jurkat cells (JC) or HCV E2-expressing Jurkat cells (384–747) which had been incubated in 100μg/ml Lck inhibitor or the vehicle control (DMSO) (D). Data represent the average of three technical replicates and the standard deviation is shown. Each experiment was repeated at least three times with consistent results. *P< 0.01.