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Bronchial Asthma and Idiopathic Pulmonary Fibrosis as Potential Targets for Hematopoietic Stem Cell Transplantation
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Júlio C. Voltarelli, Eduardo A. Donadi, José A. B. Martinez, Elcio O. Vianna, Willy Sarti
The major consequence of the activation of Th2 cells in allergic bronchial asthma is the B cell gene switch to produce IgE in response to ubiquitous environmental allergens. The initial interaction of B and Th2 cells depends on the recognition of an allergen peptide in association with an MHC class II molecule on the B cell membrane, followed by the CD28/B7 costimulation, as occurs for other APCs. Two further signals are necessary to induce the switching of antibody synthesis from IgM to IgE, the first is generated after the binding of CD40 molecule present on B cell surface to the CD40 ligand (CD 154), expressed on Th2 cells.47 The interaction of these molecules leads to activation of the nuclear transducer NFκB, one of the transcription factors required for the production of IgE.48 The activated Th2 cells secrete IL-4 and IL-13, the most important inducers of the production of IgE,47 and then, provide the second signal to the switching to IgE. The binding of IL-4 or its homolog IL-13 to specific receptors (IL4R and IL-13R, respectively) on B cell membrane leads to the activation of another transcription factor, the signal transducer and activator of transcription 6 (STAT-6).48 Once formed, IgE antibodies briefly circulate in the blood before binding to the FcεRI-α on mast cells and basophils. The cross-linking of allergens to IgEs on the membrane of mast cells and basophils triggers the release of preformed mediators, including histamine, tryptase and chymase, and newly-formed membrane-derived lipid mediators, including leukotrienes (LTA4, LTB4, LTC4, LTD4 and LTE4), prostanoids (PGD2, thromboxane A2), and platelet-activating factor.49 Mast cell-derived cysteinyl-leukotrienes (LTC4, LTD4 and LTE4) are considered to be the major mediators of the early airflow obstruction, also known as early asthmatic response, which occurs immediately after allergen exposure and subsides within one hour. Approximately half of asthmatic patients also present a four to six-hour late airflow obstruction, also known as late asthmatic response. The late response develops as a consequence of the production of cytokines and chemokines by mast cells, macrophages, epithelial cells, lymphocytes and eosinophils. Besides producing cysteinyl leukotrienes, eosinophils also contribute to the late asthmatic response by releasing granule-associated proteins such as major basic protein, eosinophil-derived neurotoxin, peroxidase and cationic proteins.1,16 In concert or individually, the myriad of preformed and newly formed mediators released after allergen exposure contributes to the development of chronic airway inflammation, airway hyperresponsiveness and bronchoconstriction, pathologic features associated with the production of respiratory crises manifest by dyspnea and wheezing.
Correlation between mast cell-mediated allergic inflammation and length of perfluorinated compounds
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Pro-inflammatory cytokines play an essential role in regulation of intracellular communications in immune response (Lacy and Stow 2011). Degranulation of mast cells is induced by binding of Ig E to high-affinity IgE receptor (FcεRI) on the surface of mast cells (Rivera and Gilfillan 2006). FcεRI is necessary to induce for IgE-mediated allergic inflammation (Galli and Tsai 2012). Cross-linking of FcεRI generates release of several inflammatory factors, which produce allergic inflammation (He et al. 2013). Previously, human mast cell line (HMC-1) stimulated by phorbol 12-myristate 13-acetate and Ca ionophore were used to study activation of mast cells (Lee et al. 2017; Singh et al. 2012). However, HMC-1 are immature and do not express FcεRI (Laidlaw et al. 2011). Daeron et al. (1995) examined IgE-FcεRI binding in degranulation of mast cells using rat basophilic leukemia cell line (RBL-2H3). Thus in the present study RBL-2H3 cells expressing FcεRI binding with IgE were employed to determine activation of mast cells.