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81.
Stephan Halle Hélène C. Dujardin Nadja Bakocevic Henrike Fleige Heike Danzer Stefanie Willenzon Yasemin Suezer Günter H?mmerling Natalio Garbi Gerd Sutter Tim Worbs Reinhold F?rster 《The Journal of experimental medicine》2009,206(12):2593-2601
Mucosal vaccination via the respiratory tract can elicit protective immunity in animal infection models, but the underlying mechanisms are still poorly understood. We show that a single intranasal application of the replication-deficient modified vaccinia virus Ankara, which is widely used as a recombinant vaccination vector, results in prominent induction of bronchus-associated lymphoid tissue (BALT). Although initial peribronchiolar infiltrations, characterized by the presence of dendritic cells (DCs) and few lymphocytes, can be found 4 d after virus application, organized lymphoid structures with segregated B and T cell zones are first observed at day 8. After intratracheal application, in vitro–differentiated, antigen-loaded DCs rapidly migrate into preformed BALT and efficiently activate antigen-specific T cells, as revealed by two-photon microscopy. Furthermore, the lung-specific depletion of DCs in mice that express the diphtheria toxin receptor under the control of the CD11c promoter interferes with BALT maintenance. Collectively, these data identify BALT as tertiary lymphoid structures supporting the efficient priming of T cell responses directed against unrelated airborne antigens while crucially requiring DCs for its sustained presence.Bronchus-associated lymphoid tissue (BALT) is part of the mucosal immune system of the lung and is characterized by the aggregation of lymphoid cells at the bifurcations of the upper bronchioles (Bienenstock and Befus, 1984). Like other lymphoid follicles, BALT is composed of B cells surrounded by a parafollicular region of T cells (Sminia et al., 1989). Recirculating lymphocytes are believed to enter BALT via high endothelial venules and leave these structures by efferent lymphatics (Lührmann et al., 2002/2003; Xu et al., 2003). Although BALT is largely absent in normal mice, it spontaneously forms in mice deficient for the chemokine receptor CCR7 (Kocks et al., 2007). In humans, it is neither found at birth nor in healthy adults but transiently arises during childhood and adolescence (Tschernig and Pabst, 2000). In both humans and mice, pulmonary infection and inflammation can induce BALT (Moyron-Quiroz et al., 2004). Data derived from splenectomized lymphotoxin-α–deficient mice, which lack all secondary lymphoid organs but do develop BALT, suggest that BALT can serve as induction sites for adaptive immune responses to pathogens with lung tropism (Moyron-Quiroz et al., 2004). However, mechanisms that control the development and maintenance of BALT are largely unknown.Modified vaccinia virus Ankara (MVA) is a highly attenuated orthopoxvirus that lost its capacity to replicate in mammalian cells (Meyer et al., 1991). Recently, MVA was proposed to represent a useful agent for mucosal vaccination via the respiratory route in a nonhuman primate model (Corbett et al., 2008). In mice, MVA delivered via the intranasal (i.n.) route has been shown to induce long-lasting and protective antibody and T cell immune responses (Gherardi and Esteban, 2005; Kastenmuller et al., 2009). However, little is known about the immunological events after respiratory MVA infection.The present report demonstrates that a single i.n. application of the replication-deficient MVA is sufficient to induce the long-lasting presence of BALT and that the lung-specific depletion of DCs interferes with BALT maintenance. Ex vivo imaging of antigen-specific T cell–DC interactions within BALT by two-photon microscopy indicates that, independent of the specific antigenic challenge inducing its formation, BALT can function as a general priming site for T cell responses directed against antigens that reach the lower respiratory tract. 相似文献
82.
83.
Amy J. Mathers Nicole Stoesser Anna E. Sheppard Louise Pankhurst Adam Giess Anthony J. Yeh Xavier Didelot Stephen D. Turner Robert Sebra Andrew Kasarskis Tim Peto Derrick Crook Costi D. Sifri 《Antimicrobial agents and chemotherapy》2015,59(3):1656-1663
The global emergence of Klebsiella pneumoniae carbapenemase-producing K. pneumoniae (KPC-Kp) multilocus sequence type ST258 is widely recognized. Less is known about the molecular and epidemiological details of non-ST258 K. pneumoniae in the setting of an outbreak mediated by an endemic plasmid. We describe the interplay of blaKPC plasmids and K. pneumoniae strains and their relationship to the location of acquisition in a U.S. health care institution. Whole-genome sequencing (WGS) analysis was applied to KPC-Kp clinical isolates collected from a single institution over 5 years following the introduction of blaKPC in August 2007, as well as two plasmid transformants. KPC-Kp from 37 patients yielded 16 distinct sequence types (STs). Two novel conjugative blaKPC plasmids (pKPC_UVA01 and pKPC_UVA02), carried by the hospital index case, accounted for the presence of blaKPC in 21/37 (57%) subsequent cases. Thirteen (35%) isolates represented an emergent lineage, ST941, which contained pKPC_UVA01 in 5/13 (38%) and pKPC_UVA02 in 6/13 (46%) cases. Seven (19%) isolates were the epidemic KPC-Kp strain, ST258, mostly imported from elsewhere and not carrying pKPC_UVA01 or pKPC_UVA02. Using WGS-based analysis of clinical isolates and plasmid transformants, we demonstrate the unexpected dispersal of blaKPC to many non-ST258 lineages in a hospital through spread of at least two novel blaKPC plasmids. In contrast, ST258 KPC-Kp was imported into the institution on numerous occasions, with other blaKPC plasmid vectors and without sustained transmission. Instead, a newly recognized KPC-Kp strain, ST941, became associated with both novel blaKPC plasmids and spread locally, making it a future candidate for clinical persistence and dissemination. 相似文献
84.
Hein J. Verberne Wanda Acampa Constantinos Anagnostopoulos Jim Ballinger Frank Bengel Pieter De Bondt Ronny R. Buechel Alberto Cuocolo Berthe L. F. van Eck-Smit Albert Flotats Marcus Hacker Cecilia Hindorf Philip A. Kaufmann Oliver Lindner Michael Ljungberg Markus Lonsdale Alain Manrique David Minarik Arthur J. H. A. Scholte Riemer H. J. A. Slart Elin Trägårdh Tim C. de Wit Birger Hesse 《European journal of nuclear medicine and molecular imaging》2015,42(12):1929-1940
85.
Michael K Schuhmann Peter Kraft Guido Stoll Kristina Lorenz Sven G Meuth Heinz Wiendl Bernhard Nieswandt Tim Sparwasser Niklas Beyersdorf Thomas Kerkau Christoph Kleinschnitz 《Journal of cerebral blood flow and metabolism》2015,35(1):6-10
While the detrimental role of non-regulatory T cells in ischemic stroke is meanwhile unequivocally recognized, there are controversies about the properties of regulatory T cells (Treg). The aim of this study was to elucidate the role of Treg by applying superagonistic anti-CD28 antibody expansion of Treg. Stroke outcome, thrombus formation, and brain-infiltrating cells were determined on day 1 after transient middle cerebral artery occlusion. Antibody-mediated expansion of Treg enhanced stroke size and worsened functional outcome. Mechanistically, Treg increased thrombus formation in the cerebral microvasculature. These findings confirm that Treg promote thrombo-inflammatory lesion growth during the acute stage of ischemic stroke. 相似文献
86.
John E. Campbell Kevin W. Kuntz Sarah K. Knutson Natalie M. Warholic Heike Keilhack Tim J. Wigle Alejandra Raimondi Christine R. Klaus Nathalie Rioux Akira Yokoi Satoshi Kawano Yukinori Minoshima Hyeong-Wook Choi Margaret PorterScott Nigel J. Waters Jesse J. Smith Richard Chesworth Mikel P. Moyer RobertA. Copeland 《ACS medicinal chemistry letters》2015,6(5):491-495
87.
88.
Carin K. Ingemarsdotter Laura A. Tookman Ashley Browne Katrina Pirlo Rosalind Cutts Claude Chelela Karisma F. Khurrum Elaine Y.L. Leung Suzanne Dowson Lee Webber Iftekhar Khan Darren Ennis Nelofer Syed Tim R. Crook James D. Brenton Michelle Lockley Iain A. McNeish 《Molecular oncology》2015,9(4):791-805
89.