Dendritic cells (DC) derived from bone marrow are critical in the function of the immune system, for they are the primary antigen-presenting cells in the activation of T-lymphocyte response. Their differentiation from precursor cells has not been defined at a molecular level, but recent studies have shown an association between expression of the relB subunit of the NF-kappa B complex and the presence of DC in specific regions of normal unstimulated lymphoid tissues. Here we show that relB expression also correlates with differentiation of DC in autoimmune infiltrates in situ, and that a mutation disrupting the relB gene results in mice with impaired antigen-presenting cell function, and a syndrome of excess production of granulocytes and macrophages. Thymic UEA-1+ medullary epithelial cells from normal mice show striking similarities to DC and, interestingly, these cells are also absent in relB mutant mice. Taken together, these results suggest that relB is critical in the coordinated activation of genes necessary for the differentiation of two unrelated but phenotypically similar cells (DC and thymic UEA-1+ medullary epithelial cells) and is therefore a candidate for a gene determining lineage commitment in the immune system.
Immunization leads to the generation of both antibody-forming cells (AFC) and memory B cells which are thought to arise in germinal centers within lymphoid follicles. The findings that the precursors to memory B cells reside in the J11Dlo subpopulation of the spleens in non-immune mice and that this subpopulation is distinct from conventional AFC precursors, including CD5+ B cells, suggest that the precursors of germinal centers might also reside in the J11Dlo subpopulation. To test this hypothesis, SCID mice were repopulated with CD4+ carrier-primed T cells and T-depleted J11Dlo, J11Dhi or CD5+ B cells and immunized with a hapten-carrier conjugate. Only the J11Dlo population was enriched for cells that produced germinal centers. Thus, the subpopulation of precursors that generates memory B cells also originates germinal centers.
Mead is a traditional drink obtained from diluted honey with the appropriate yeast inoculations. However, the production of mead is time-consuming, and the process often takes several months to accomplish. During the elaboration of mead, sluggish and stuck fermentations often occur and lead to the production of undesirable flavours. To improve the condition of longan mead production in Taiwan, multiple yeast inoculations with different strains of yeast were examined in this study. The physicochemical properties and mead aroma compounds were measured. Longan mead without multiple inoculations, but with added yeast nutrients, displayed a sharp increase in ethanol content compared with the inoculated groups without yeast nutrients. However, the physicochemical properties of every mead reached almost the same endpoint at the end of the fermentation time (day 22). Moreover, differences among the groups were observed in their aroma compounds. Some aroma compounds, such as 2-methyltetrahydrothiophen-3-one, 1-propanol and 2-methylbutyl acetate, were only found in the double-inoculation groups, whereas other aroma compounds, such as phenethyl acetate and linalool, were only found in the single-yeast inoculation groups. These results demonstrate that multiple inoculations have a positive effect on longan mead fermentation. This technique could assist local producers in elaborating a longan mead of acceptable quality.
Vasoactive intestinal peptide (VIP) is a neuroendocrine mediator in immune tissues that affects many T cell functions through two homologous high‐affinity G‐protein‐coupled receptors, termed VIPR1 and VIPR2. Antigen‐stimulated secretion of γ‐interferon (IFN‐γ) by sperm whale myoglobin‐specific Th1 cells of DBA/2 mouse I‐Ed‐restricted clones, which express VIPR1 and VIPR2, was enhanced by 10−10 M to 10−7 M VIP. Enhancement of IFN‐γ secretion reached a mean maximum of fourfold for VIP and threefold for a VIPR2‐selective agonist, without any effect of a VIPR1‐selective agonist. Secretion of IFN‐γ by PMA and ionomycin‐stimulated clones of Th1 cells was not altered by VIP. Antigen‐stimulated secretion of IFN‐γ by T cell receptor‐transgenic, influenza hemagglutinin‐specific, and cytokine‐differentiated mouse lymph node Th1 cells, which also express VIPR1 and VIPR2, was enhanced by 10−10 M to 10−8 M VIP. Enhancement of IFN‐γ secretion increased to a maximum of 14‐fold for VIP, 14‐fold for the VIPR2‐selective agonist, and 20‐fold for the VIPR1‐selective agonist. In contrast to VIP suppression of interleukin production and lack of effect on IFN‐γ production by T cells stimulated with anti‐CD3 antibody or a mitogenic lectin, generation of IFN‐γ by antigen‐stimulated T cells is enhanced significantly by physiological concentrations of VIP.—Jabrane‐Ferrat, N., Bloom, D., Wu, A., Li, L., Lo, D., Sreedharan, S. P., Turck, C. W., Goetzl, E. J. Enhancement by vasoactive intestinal peptide of γ‐interferon production by antigen‐stimulated type 1 helper T cells. FASEB J. 13, 347–353 (1999)
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