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Titlebook: Recent Advances in Mucosal Immunology; Part A: Cellular Int Jiri Mestecky,Jerry R. McGhee,Pearay L. Ogra Book 1987 The Editor(s) (if applic

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Novel Regulatory Mechanisms of IgA Synthesis: Respective Roles of Neuropeptides and Cells of the Antstence of a specific mechanism to facilitate the transport of IgA across the epithelium into secretions (5). In this paper, we report our data concerning two other mechanisms that may be capable of enhancing IgA production, namely neuropeptides and the antisuppressor regulatory circuit.
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Isotype Specific Immunoregulation: Role of FcαR+ T Cells and IBFα in IgA ResponsescεR) occur on T cells which regulate this isotype response via production of either enhancing or suppressive IgE binding factors (IBFε) (3). Both potentiating and suppressive IBFε are similar in size (Mr ~15,000). They contain a common protein core, and the degree of glycosylation determines whether IBFε enhances or suppresses the IgE responses.
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Antigen-Specific Helper T Cells in the Intestine: Origin and Migrationnumber of different factors. Some studies have used cloned T cells but the fact that some cloned cells lose surface receptors and display abberrant migratory behaviour (9) is a concern with these models.
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Limiting Dilution Analysis of Functional T Cells in the Gut Mucosahat many IEL are thymus-independent, contain granules and are Thy-1. (3–6). Indeed, we have recently shown by limiting dilution analysis that 1 in about 170 of normal mouse IEL are mast cell precursors, and that the frequency can reach as high as 1 in 60 if the mice are worm infected (7).
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Rabbit IgA Heavy Chain Genes: Cloning and , Expression since both mouse and human have only one and two Ca genes, respectively. Genomic blot data are consistent with studies of rabbit IgA heavy chain allotypes which suggested the existence of multiple IgA isotypes (2–4), To further examine the complexity and genetic control of rabbit IgA, we have under
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Immunoglobulin Gene Expression in Wasted Miceabnormalities and immunodeficiency. The disease produced by this spontaneous autosomal recessive mutation (.) is phenotypically manifested in homozygous ./. mice at three weeks of age as a neurologic abnormality. The animals develop tremor and uncoordinated movements which is followed by progressive
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Molecular Aspects of T Cell Regulation of B Cell Isotype Differentiationsuch as Peyer’s patches, have a greater tendency to become IgA B cells, than B cells in other developmental areas. One theory is based on the supposition that surface IgM-bearing (mIgM-bearing) B cells in the mucosal follicles are more subject to antigen stimulation than cells in other areas and the
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Switch T Cell Line, ST, Induces an Ig Class Switch in Surface Isotype in B cells derived from patients with immunodeficiency and hyper-IgM (1,2). Previously, it had been postulated that the defect in these patients was intrinsic to the B cell, being incapable of switching from p to y or a (3,4). However, we have now studied 13 such patients with 11 able to secrete Ig
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