2 resultados para Th pathways
em Bucknell University Digital Commons - Pensilvania - USA
Resumo:
Potential energy curves have been calculated for CnH22+ (n = 2−9) ions and results have been compared with data on unimolecular charge-separation reactions obtained by Rabrenović and Beynon. Geometry-optimized, minimum energy, linear CnH22+ structures have been computed for ground and low-lying excited states. These carbodications exist in stable configurations with well depths greater than 3 eV. Decomposition pathways into singly charged fragment ions lead to products with computed kinetic energies in excess of 1 eV. A high degree of correlation exists between experimental information and results computed for linear CnH22+ structures having hydrogen atoms on each end. The exception involves C4H22+reactions where a low-lying doubly charged isomer must be invoked to rationalize the experimental data.
Resumo:
Calcineurin-inhibitor refractory bronchiolitis obliterans (BO) represents the leading cause of late graft failure after lung transplantation. T helper (Th)2 and Th17 lymphocytes have been associated with BO development. Taking advantage of a fully allogeneic trachea transplantation model in mice, we addressed the pathogenicity of Th cells in obliterative airway disease (OAD) occurring in cyclosporine A (CsA)-treated recipients. We found that CsA prevented CD8+ T cell infiltration into the graft and downregulated the Th1 response but affected neither Th2 nor Th17 responses in vivo. In secondary mixed lymphocyte cultures, CsA dramatically decreased donor-specific IFN-γ production, enhanced IL-17 production and did not affect IL-13. As CD4+ depletion efficiently prevented OAD in CsA-treated recipients, we further explored the role of Th2 and Th17 immunity in vivo. Although IL-4 and IL-17 deficient untreated mice developed an OAD comparable to wild-type recipients, a single cytokine deficiency afforded significant protection in CsA-treated recipients. In conclusion, CsA treatment unbalances T helper alloreactivity and favors Th2 and Th17 as coexisting pathways mediating chronic rejection of heterotopic tracheal allografts.