作者: Tanja Schreiber , Stefan Ehlers , Sahar Aly , Alexandra Hölscher , Sven Hartmann
DOI: 10.4049/JIMMUNOL.176.2.1131
关键词:
摘要: Immunity to Mycobacterium tuberculosis infection is critically dependent on the timely priming of T effector lymphocytes and their efficient recruitment site mycobacterial implantation in lung. E-, P-, L-selectin counterreceptors control lymphocyte homing lymph nodes leukocyte trafficking peripheral sites acute inflammation, adhesive function depending fucosylation by fucosyltransferases (FucT) IV VII. To address relative importance differentially glycosylated selectin for cell functions a model mycobacteria-induced granulomatous pulmonary we used aerosol-borne M. infect FucT-IV-/-, FucT-VII-/-, FucT-IV-/-/FucT-VII-/-, or wild-type mice. In nodes, infected FucT-IV-/-/FucT-VII-/- and, lesser extent, FucT-VII-/- mice had severely reduced numbers cells Ag-specific responses. By contrast, activated into lungs was similar all four groups during expression cell, macrophage were only delayed Importantly, from expressed CXCL13, CCL21, CCL19 displayed organized follicular neolymphoid structures after with tuberculosis, which suggests that lung served as ligand-independent immune responses infection. All FucT-deficient strains fully capable restricting growth organs until at least 150 days postinfection. Our observations indicate dictated FucT-IV FucT-VII-dependent ligand activities are not critical inducing maintaining levels necessary tuberculosis.