Blood ACTH levels following subcutaneous injections.
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In situ staining techniques were used to visualize physical interactions between dendritic cell subsets and naive Ag-specific CD4 T cells in the lymph node. Before injection of Ag, CD8(+) dendritic cells and naive OVA-specific CD4 T cells were uniformly distributed throughout the T cell-rich paracortex, whereas CD11b(+) dendritic cells were located mainly in the outer edges of the paracortex near the B cell-rich follicles. Many OVA-specific CD4 T cells were in contact with CD8(+) dendritic cells in the absence of OVA. Within 24 h after s.c. injection of soluble OVA, the OVA-specific CD4 T cells redistributed to the outer paracortex and interacted with CD11b(+), but not CD8(+) dendritic cells. This behavior correlated with the uptake of OVA and the presence of peptide-MHC complexes on the surface of CD11b(+) dendritic cells, and subsequent IL-2 production by the Ag-specific CD4 T cells. These results are consistent with the possibility that CD11b(+) dendritic cells play a central role in the activation of CD4 T cells in response to s.c. Ag.
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Experiments were conducted on guinea pigs. With the aid of fluorescein-labeled antibodies it was shown that following a single or a two-fold immunization into the footpad complete typhoid antigen was revealed in the lung macrophages as soon as the first days (or after a two-fold administration-in several hours) and persisted there for 30 days. There was a tendency to concentration of the antigen-containing macrophages in the perivascular and the peribronchial tissues. The dynamics of the antigen spread along the lymphoid organs is also described.
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PEG-Intron is a covalent conjugate of recombinant alpha-2b interferon with monomethoxy polyethylene glycol (PEG). Compared to standard interferon-alpha injections, this preparation has a longer half-life allowing for once-weekly injections and superior antiviral efficacy in the treatment of hepatitis C when used in combination with ribavirin. We report the first case of a local blistering reaction developing in a patient receiving pegylated interferon-alpha-2b. Previous reports of local cutaneous reactions to standard and pegylated interferon-alpha are reviewed and the pathophysiological mechanisms are discussed.
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