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- Matsuzaki, G, et al.
(författare)
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Mechanism of murine V gamma 1(+) gamma delta T cell-mediated innate immune response against Listeria monocytogenes infection
- 2002
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Ingår i: European Journal of Immunology. - 1521-4141. ; 32:4, s. 928-935
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Tidskriftsartikel (refereegranskat)abstract
- Murine gammadelta T cells participate in innate immune response against infection of the intracellular bacterium Listeria monocytogenes. In the present report, we analyzed the mechanism of the gammadelta T cell-mediated response against L. monocytogenes infection. gammadelta T cell-enriched spleen cells of L. monocytogenes-infected mice produced IFN-gamma in vitro in response to L. monocytogenes-infected spleen cells, The IFN-gamma production was abrogated by depletion of Vgamma1(+) gammadelta T cells. IFN-gamma production of the Vy1(+) gammadelta T cells in response to L. monocytogenes-infected spleen cells required IL-12. However, addition of Fab fragment of anti-TCR gammadelta monoclonal antibodies (mAb) failed to block the response, suggesting that the response requires no TCR-mediated antigen recognition. Interestingly, Vgamma1(+) gammadelta T cells of naive mice also produced IFN-gamma in response to L. monocytogenes-infected spleen cells in an IL-12-dependent manner. Furthermore, the IL-12 receptor (IL-12R) gene was expressed on the Vgamma1(+) gammadelta T cells of naive mice as well as those of L. monocytogenes-infected mice although naive alphabeta T cells lack IL-12R expression. All the results suggest that the Vgamma1(+) gammadelta T cells participate in immune surveillance against intracellular bacterial infection through quick production of IFN-gamma in response to infection-induced IL-12 without antigen-driven clonal expansion and maturation.
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- Yoshihara, S., et al.
(författare)
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Long-lasting smooth-muscle relaxation by a novel PACAP analogue in human bronchi
- 2004
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Ingår i: Regul Pept. ; 123:1-3
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Tidskriftsartikel (refereegranskat)abstract
- We compared the relaxant effect of original pituitary adenylate cyclase-activating peptide (PACAP)1-27 with that of a newly developed, synthetic PACAP1-27 analogue, [Arg(15,20,21) Leu(17)]-PACAP-Gly-Lys-Arg-NH(2), in human bronchi in vitro (n=4-5 in each group). Using precontraction by carbachol (0.1 muM), cumulative administration of PACAP1-27 and salbutamol caused concentration-dependent smooth muscle relaxation with similar potencies and maximum relaxant effects. Non-cumulative administration of the PACAP1-27 analogue and the original PACAP1-27 caused concentration-dependent relaxation with a similar maximum relaxant effect and potency as well. However, the onset and offset of action was markedly slower for the PACAP1-27 analogue than for the original PACAP1-27 (>90% versus <10% of peak relaxation remaining 5 h after administration). Peptidase inhibition by captopril (10 muM) and phosphoramidon (1 muM) significantly increased the maximum relaxant effect and duration of action of PACAP1-27 but not of the PACAP1-27 analogue, during the 3 h of observation in the human bronchi. We conclude that [Arg(15,20,21) Leu(17)]-PACAP-Gly-Lys-Arg-NH(2) produces significant concentration-dependent and sustained bronchial smooth muscle relaxation in vitro. The sustained relaxant effect is due, at least in part, to the synthetic PACAP1-27 analogue being less susceptible to cleavage by peptidases than the original peptide PACAP1-27.
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