This confirmed

that sG helps wt RSV evade the antibody-dependent restriction of replication but indicated that in mice, it is not acting primarily as a decoy for G-specific antibodies, perhaps because sG is produced in insufficient quantities in this poorly permissive animal. Rather, we found that the greater sensitivity of mG versus Tozasertib wt RSV to the antiviral effect of passively transferred RSV antibodies required the presence of inflammatory cells in the lung and was Fc gamma receptor dependent. Thus, sG helps RSV escape the antibody-dependent restriction of replication via effects as an antigen decoy and as a modulator of leukocytes bearing Fc gamma receptors.”
“The present Study was designed to determine whether the p53 tumor-suppressor Protein is involved in the development of antinociceptive tolerance to morphine. When the doses of morphine(mg/kg per injection) were

selleckchem subcutaneously given into mice as pretreatment twice daily for 2 days (first day (30) and second day (60)), intrathecal (i.t.) administration of morphine (0.1 nmol) was inactive due to antinociceptive tolerance in the 0.5% formalin test on the third day. Tolerance to i.t. morphine was significantly suppressed by i.t. injection of pifithrin-alpha (1 and 10 nmol), an inhibitor of p53 activation, benzyloxycarbonyl-Val-Ala- Asp(OMe)-fluoromethylketone (Z-VAD-fmk) (1 and 10 nmol), a non-selective caspase inhibitor, or N(G)- nitro-L-arginine methyl ester(L-NAME)(2 and 20 nmol), a non-selective inhibitor of nitric oxide synthase, 5 min before each morphine treatment during the pentoxifylline induction, With none given on the test day. Moreover, p53 expression in the spinal cord had increased

significantly 14 h after the last morphine administration. These results indicate that the increased expression and activation of p53, and the nitric oxide and caspase systems related to p53 may contribute to the development of antinociceptive tolerance to morphine in the mouse spinal cord. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Infection of mice with murine gammaherpesvirus 68 (MHV-68) robustly activates CD8 T cells, but only six class I major histocompatibility complex (MHC)-restricted epitopes have been described to date for the widely used H-2(b) haplotype mice. To explore the specificity and kinetics of the cytotoxic T-lymphocyte response in MHV-68-infected C57BL/6 mice, we screened for H-2K(b)- and H-2D(b)- restricted epitopes using a set of 384 candidate epitopes in an MHC tetramer-based approach and identified 19 new epitopes in 16 different open reading frames. Of the six known H-2K(b)- and H-2D(b)- restricted epitopes, we confirmed a response against three and did not detect CD8 T-cell-specific responses for the remaining three. The peak of the CD8 T-cell response to most peptides occurs between 6 and 10 days postinfection.