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    Airway responsiveness in CD38-deficient mice in allergic airway disease: studies with bone marrow chimeras (2015)
    The American Physiological Society (APS)
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    Publication Date: 2015-03-02
    Description: CD38 is a cell-surface protein involved in calcium signaling and contractility of airway smooth muscle. It has a role in normal airway responsiveness and in airway hyperresponsiveness (AHR) developed following airway exposure to IL-13 and TNF-α but appears not to be critical to airway inflammation in response to the cytokines. CD38 is also involved in T cell-mediated immune response to protein antigens. In this study, we assessed the contribution of CD38 to AHR and inflammation to two distinct allergens, ovalbumin and the epidemiologically relevant environmental fungus Alternaria. We also generated bone marrow chimeras to assess whether Cd38 +/+ inflammatory cells would restore AHR in the CD38-deficient ( Cd38 –/– ) hosts following ovalbumin challenge. Results show that wild-type (WT) mice develop greater AHR to inhaled methacholine than Cd38 –/– mice following challenge with either allergen, with comparable airway inflammation. Reciprocal bone marrow transfers did not change the native airway phenotypic differences between WT and Cd38 –/– mice, indicating that the lower airway reactivity of Cd38 –/– mice stems from Cd38 –/– lung parenchymal cells. Following bone marrow transfer from either source and ovalbumin challenge, the phenotype of Cd38 –/– hosts was partially reversed, whereas the airway phenotype of the WT hosts was preserved. Airway inflammation was similar in Cd38 –/– and WT chimeras. These results indicate that loss of CD38 on hematopoietic cells is not sufficient to prevent AHR and that the magnitude of airway inflammation is not the predominant underlying determinant of AHR in mice.
    Print ISSN: 1040-0605
    Electronic ISSN: 1522-1504
    Topics: Medicine
    Published by The American Physiological Society (APS)
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  • 2
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    Blimp-1-dependent and -independent natural antibody production by B-1 and B-1-derived plasma cells (2017)
    Rockefeller University Press
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    Publication Date: 2017-09-05
    Description: Natural antibodies contribute to tissue homeostasis and protect against infections. They are secreted constitutively without external antigenic stimulation. The differentiation state and regulatory pathways that enable continuous natural antibody production by B-1 cells, the main cellular source in mice, remain incompletely understood. Here we demonstrate that natural IgM-secreting B-1 cells in the spleen and bone marrow are heterogeneous, consisting of (a) terminally differentiated B-1–derived plasma cells expressing the transcriptional regulator of differentiation, Blimp-1, (b) Blimp-1 + , and (c) Blimp-1 neg phenotypic B-1 cells. Blimp-1 neg IgM-secreting B-1 cells are not simply intermediates of cellular differentiation. Instead, they secrete similar amounts of IgM in wild-type and Blimp-1–deficient (PRDM-1 Ex1A ) mice. Blimp-1 neg B-1 cells are also a major source of IgG3. Consequently, deletion of Blimp-1 changes neither serum IgG3 levels nor the amount of IgG3 secreted per cell. Thus, the pool of natural antibody-secreting B-1 cells is heterogeneous and contains a distinct subset of cells that do not use Blimp-1 for initiation or maximal antibody secretion.
    Print ISSN: 0022-1007
    Electronic ISSN: 1540-9538
    Topics: Medicine
    Published by Rockefeller University Press
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  • 3
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    B Lymphocytes Are Required during the Early Priming of CD4+ T Cells for Clearance of Pneumocystis Infection in Mice [INFECTIOUS DISEASE AND HOST RESPONSE] (2015)
    The American Association of Immunologists (AAI)
    Details
    Publication Date: 2015-07-03
    Description: B cells play a critical role in the clearance of Pneumocystis . In addition to production of Pneumocystis -specific Abs, B cells are required during the priming phase for CD4 + T cells to expand normally and generate memory. Clearance of Pneumocystis was found to be dependent on Ag specific B cells and on the ability of B cells to secrete Pneumocystis -specific Ab, as mice with B cells defective in these functions or with a restricted BCR were unable to control Pneumocystis infection. Because Pneumocystis -specific antiserum was only able to partially protect B cell–deficient mice from infection, we hypothesized that optimal T cell priming requires fully functional B cells. Using adoptive transfer and B cell depletion strategies, we determined that optimal priming of CD4 + T cells requires B cells during the first 2–3 d of infection and that this was independent of the production of Ab. T cells that were removed from Pneumocystis -infected mice during the priming phase were fully functional and able to clear Pneumocystis infection upon adoptive transfer into Rag1 –/– hosts, but this effect was ablated in mice that lacked fully functional B cells. Our results indicate that T cell priming requires a complete environment of Ag presentation and activation signals to become fully functional in this model of Pneumocystis infection.
    Print ISSN: 0022-1767
    Electronic ISSN: 1550-6606
    Topics: Medicine
    Published by The American Association of Immunologists (AAI)
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