Basic and clinical immunologySusceptibility to allergic lung disease regulated by recall responses of dual-receptor memory T cells∗
Section snippets
Animals
DO-11.10 mice (BALB/c) transgenic for a TCR recognizing ovalbumin peptide 323-33914 and influenza A hemaglutinin (HNT) mice (BALB/c) transgenic for a TCR recognizing HNT peptide from the influenza A hemagglutinin protein15 were bred in the Vanderbilt University Medical School or in the Cleveland Clinic Foundation mouse facility. Immunocompetent, nonirradiated BALB/c transfer recipients were females 4 to 8 weeks old from Jackson Laboratory (Bar Harbor, Me). All mice were maintained in specific
DualR memory TH1 cells can abrogate AHR when present before a TH2-inducing stimulus
Mice transgenic for the ovalbumin-specific DO-11.10 TCR, identified by using the anticlonotypic antibody KJ1-26, were mated with animals expressing an I-Ad-restricted TCR recognizing the influenza hemagglutinin peptide HNT, identified by using the Vβ8.3 TCR chain.14., 15. This receptor pair was physically compatible at the cell surface, as evidenced by flow-cytometric staining (see Fig E1, A, in the Journal's Online Repository at www.mosby.com/jaci), and no apparent abnormalities of thymic
Discussion
In considering the pathogenesis of asthma, the role of respiratory infections is pertinent because they precipitate most disease flares.6., 7., 25., 26., 27. Moreover, microbial infections in childhood may influence the susceptibility to later development of atopic asthma.3., 4. However, there is a paucity of experimental data directed toward explaining the potential mechanisms of these clinical observations. The current findings provide evidence of one means by which the immunologic repertoire
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Supported by grants from the National Heart, Lung, and Blood Institute (R01 HL61752 to Dr Boothby; K08 HL04449 to Dr Aronica), an American Lung Association Fellowship (Dr Aronica), and the Sandler Program for Asthma Research (01-0069), and by access to the core facilities of Vanderbilt University (supported by P60DK20593 and CA68485).
Because memory T cells are sometimes confused with a steady-state CD44hi or CD45RBlo population, which is composed of a variety of subsets including currently activated effector T cells and natural killer T cells, the current work refers to rested (in the absence of antigen), antigen-experienced T cells as memory T cells, as opposed to (currently activated) effectors.