In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Q: Context: To determine whether repeat administration of an adenovector (Ad) into the eye results in efficient gene delivery and to test whether transgenes can be expressed from an adenovector expression system in the presence of preexisting, neutralizing anti-Ad antibodies.', 'To assess the efficiency of repeated gene delivery of an adenovector expression system, C57Bl/6 mice received one, two, or three injections (intravitreal [IVT] or periocular [PO]) of AdNull.11D (empty cassette) at 2-week intervals, followed by a single AdLuciferase (AdL.11D) IVT or PO injection. Mice were killed approximately 24 hours after AdL.11D injection and the eyes were enucleated and stored until assayed. Serum samples were also analyzed to determine whether repeated IVT or PO injections lead to induction of neutralizing antibodies directed against an adenovector delivery system. To determine whether preexisting neutralizing anti-Ad antibodies would block transgene expression, mice were preimmunized with one, two, or three intramuscular (IM) injection(s) of AdNull.11D (1 x 10(9) particle units [pu]). Fourteen days later, when systemic anti-Ad antibody titers were expected to exist, mice were given a single AdL.11D injection (IVT or PO) and killed, and the eyes and serum collected.', 'These studies show that multiple injections at 2-week intervals with adenovectors (IM, IVT, or PO) did not prevent transgene expression in the eye. Moreover, measurement of neutralizing anti-Ad antibody titers revealed that measurable anti-Ad antibody titers in mice did not ablate transgene expression.\Question: Does repeated administration of adenovector in the eye result in efficient gene delivery?

A: These studies suggest that transgene expression after repeated adenovector administration into the eye is feasible and repeated injections, whether given IVT or PO, do not lead to an immediate increase in neutralizing anti-Ad antibody titers. Moreover, preimmunization of mice by systemic exposure to adenovector, does not block transgene expression in the eye. These studies indicate that repeat administration of adenovectors (IVT and PO) into the eye can be considered in designing future clinical trials and that the pre-existence of neutralizing anti-Ad antibodies probably does not mitigate activity.
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Q: Context: High arginase-1 (Arg) expression by myeloid-derived suppressor cells (MDSC) is known to inhibit antitumor T-cell responses through depletion of l-arginine. We have previously shown that nitric oxide (NO), an immune mediator produced from l-arginine, is a potent radiosensitizer of hypoxic tumor cells. This study therefore examines whether Arg(+) overexpressing MDSC may confer radioresistance through depleting the substrate for NO synthesis.', 'MDSC and Arg expression were studied in preclinical mouse CT26 and 4T1 tumor models and further validated in rectal cancer patients in comparison with healthy donors. The radioprotective effect of MDSC was analyzed in hypoxic tumor cells with regard to l-arginine depletion.', 'In both mouse tumors and cancer patients, MDSC expansion was associated with Arg activation causing accelerated l-arginine consumption. l-Arginine depletion in turn profoundly suppressed the capacity of classically activated macrophages to synthesize NO resulting in impaired tumor cell radiosensitivity. In advanced cT3-4 rectal cancer, circulating neutrophils revealed Arg overexpression approaching that in MDSC, therefore mounting a protumor compartment wherein Arg(+) neutrophils increased from 17% to over 90%.\Question: Do myeloid-derived suppressor cells reveal radioprotective properties through arginase-induced l-arginine depletion?

A: Protumor Arg(+) MDSC reveal a unique ability to radioprotect tumor cells through l-arginine depletion, a common mechanism behind both T-cell and macrophage inhibition.
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Q: Context: Constitutive expression and upregulation of FasL by malignant epithelial cells counterattack infiltrating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) and induce apoptosis of normal cells within the tumor, which may induce metastasis. As little is known about the mechanisms that regulate expression of Fas ligand and the subsequent release of FasL in epithelial ovarian cancer cells (EOC), we investigated the effects of lysophosphatidic acid (LPA) on FasL expression and associated signaling pathways.', 'We used established EOC cell lines that were incubated with or without LPA and FasL expression was detected by flow cytometry. Cells were additionally lysed and detected for total protein expression. Activated CD4+ T cells, after coculture with or without EOC, were collected for apoptosis staining and analysis by flow cytometry.', 'Flow cytometry showed that LPA strongly upregulated FasL expression on the OVCAR3 cell surface (P < 0.01), yet in Dov13 cells, LPA significantly upregulated FasL expression only in the presence of the general matrix metalloproteinase (MMP) inhibitors GM6001 and MMP inhibitor II (P < 0.01). The MEK/ERK1/2 kinase cascade is required for FasL upregulation, since the MEK inhibitor PD98059 significantly inhibited FasL upregulation induced by LPA (P < 0.01). Type II secretory phospholipase A2 (sPLA2-II), which promotes protein exocytosis from secretory vesicles and gelatinase granules, affects FasL translocation from intracellular to the cell surface. Pretreatment of Dov13 cells with LPA increased activated T cell apoptosis in cocultures.\Question: Does upregulation of FasL by LPA on ovarian cancer cell surface lead to apoptosis of activated lymphocytes?

A:
These data suggest that upregulation of FasL by LPA provides EOC immune-privilege and leads to apoptosis of activated T lymphocytes.
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