ABSTRACT
The finite size effect of proton conductivity of amorphous aluminosilicate thin films, a-Al(n)Si(1-n)O(x) (n = 0.07, 0.1, 0.2, 0.3 and 0.45), prepared by a sol-gel process was investigated by experimental and numerical techniques. High-resolution TEM clarified that a-Al(n)Si(1-n)O(x) films had the heterogeneous nanoscale microstructures comprised of the ion-conducting, condensed glass microdomain and the poor-conductive, uncondensed glass microdomain. σ of the films with n≤0.1 exponentially increased upon decreasing thickness in the sub-100 nm range because the volume fraction of conductive domains was less than the percolation threshold and cluster size scaling of the conductive domain was operative. The numerical simulation suggested that conductance of the condensed domain was higher than that of the uncondensed domain by 2 orders of magnitude. Volume fractions of the condensed domain increased with increasing Al/Si molar ratio and were over the percolation threshold (24.5%) with n≥0.2. However, conductance of the condensed domain decreased with increasing Al/Si ratio with n≥0.2 because the aluminosilicate glass framework made of 4-fold-connected MO(4) tetrahedra was deformed by forming the octahedral AlO(6) moieties, as checked by Al K-edge XAS. It was found that the optimal Al/Si composition in terms of the conductance of the condensed domain is not in coincidence with that in terms of the average conductivity of the films.
ABSTRACT
Acute graft-versus-host disease (a-GVHD) is initiated primarily by immunologically competent cytotoxic T cells (CTLs) that express anti-host specificities. However, the host lymphoid compartment in which these precursor CTLs are initially stimulated remains unclear. Here we show that gut Peyer's patches (PPs) are required to activate anti-host CTL responses in a well characterized murine acute graft-versus-host reaction (a-GVHR) model, involving transfer of parent lymphocytes into F1 hybrid recipients. The a-GVHR was prevented when recruitment of donor T cells into PP was interrupted either by disrupting the gene encoding chemokine receptor CCR5 or by blocking integrin alpha(4)beta(7)-MAdCAM-1 (mucosal vascular addressin) interactions. Mice deficient for PPs failed to develop a-GVHD in two models of disease induction. Thus, blockade of CTL generation in PPs might offer new strategies for circumventing a-GVHD.
Subject(s)
Cell Adhesion Molecules , Graft vs Host Disease/etiology , Graft vs Host Reaction , Peyer's Patches/immunology , Acute Disease , Animals , CD8-Positive T-Lymphocytes/immunology , Disease Models, Animal , Graft vs Host Disease/immunology , Graft vs Host Disease/prevention & control , Immunoglobulins , Interferon-alpha/antagonists & inhibitors , Mice , Mice, Inbred C3H , Mice, Inbred C57BL , Mice, Inbred DBA , Mice, Knockout , Models, Immunological , Mucoproteins/antagonists & inhibitors , Receptors, CCR5/deficiency , Receptors, CCR5/genetics , T-Lymphocytes, Cytotoxic/immunologyABSTRACT
AIM:To isolate mouse CCR5 cDNA (muCCR5) and study its expression in vivo.METHODS: Marathon PCR was used to isolate muCCR5 cDNA and two animal models were designed to investigate the gene expression in vivo, one was mouse fulminant hepatitis induced by Propionibacterium acnes (P.acnes) and the other was that with delayed type hypersensitivity reaction (DTH). A specific GST-NH2-terminus of muCCR5 fusion protein antibody F(ab')(2) was prepared and clarified. RT-PCR and immunohistochemical analysis were used to observe the expression level of CCR5 gene in mice.RESULTS: A positive reaction of mouse macrophage was found in DTH but not expressed in P.acnes induced fulminant hepatitis by RT-PCR and immunohistochemical analysis.CONCLUSION: This muCCR5 expression may be involved in an allergic processmediated by cellular immunity but not acute inflammatory reaction induced by P.acnes.
