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Functional consequences of chronic mast cell activation by aged mesenteric lymphatic vessels (666.1)
Author(s) -
Gashev Anatoliy,
Chatterjee Victor,
Tobin Richard,
Newell Rogers M. Karen
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.666.1
Subject(s) - degranulation , immune system , lymphatic system , immunoglobulin e , immunology , inflammation , medicine , mhc class ii , lymphangiogenesis , biology , t cell , receptor , antibody , cancer , metastasis
Here we present novel data related to interactions between lymphatic vessels, mast cells (MCs), eosinophils, and immune cells. MCs are known to inhabit in greater density the tissue near mesenteric lymphatic vessels (MLVs). Acute activation induces MC degranulation with subsequent recruitment of eosinophils and of MHC class II+ cells towards MLVs. Aging permanently influences mesenteric MCs by inducing chronic basal activation, thereby influencing contractility of aged MLVs. At the same time, the number of intact MCs available to react acutely to inflammatory stimuli decreases with age. The diminished number and activity of MCs in aged tissues also diminishes traffic and activation of eosinophils and other immune cells that are attracted to aged MLVs. Concurrently, MCs can function as helper cells for B cells that can produce IgE. IgE has a relatively short half‐life in the absence of chronic MC activation. We propose that a key component of aging‐associated alterations of “mesenteric lymphatic system‐mast cells/eosinophils‐inflammatory cells” system is the increased basal activation of resident MCs and eosinophils in aged mesentery that promote chronic inflammation while being insufficient to recruit enough anti‐inflammatory MHC class II+ cells and eosinophils, resulting in the inability to prevent a smooth transition from acute inflammation to specific immune cell activation. NIH R01 AG030578. Grant Funding Source : NIH R01 AG030578