TAP2-DEFECTIVE RMA-S CELLS PRESENT SENDAI VIRUS-ANTIGEN TO CYTOTOXIC T-LYMPHOCYTES

The murine antigen-processing-defective mutant cell line RMA-S is leak y in the presentation of certain endogenously synthesized minor histoc ompatibility and viral antigens to major histocompatibility complex (M HC) class I-restricted cytotoxic T lymphocytes (CTL). The viral antige ns include influenza virus nucleoprotein, vesicular stomatitis virus ( VSV) nucleocapsid and Rauscher murine leukemia virus (MuLV) antigen. H ere we demonstrate Sendai virus antigen presentation by the HAM2 (muri ne TAP2, transporter associated with antigen presentation type 2)-defe ctive RMA-S cell line and compare antigen presentation after restorati on of the defect by murine TAP1/2 gene transfection. Kinetic studies r evealed that RMA-S cells required 2-3 h longer incubation and approxim ately 10 times higher doses of Sendai virus to reach the same level of killing as the RMA parental line. After transfection of RMA-S cells w ith the murine TAP1/2 gene, Sendai virus antigen presentation was rest ored to levels of the RMA wild-type line with regard to time of virus infection and dose of virus needed for sensitizing target cells. The p resentation of Sendai virus antigen in RMA-S cells was sensitive to br efeldin A (BFA), suggesting that the presentation was mediated.via the endogenous pathway. Our findings comfirmed leakiness of antigen prese ntation in RMA-S cells and extended it to Sendai virus. The results un derscored the role for intact expression of the TAP 1/2 molecules for efficient MHC class I-mediated antigen presentation.