University of Hamburg

About: University of Hamburg is a education organization based out in Hamburg, Germany. It is known for research contribution in the topics: Population & Laser. The organization has 45564 authors who have published 89286 publications receiving 2850161 citations. The organization is also known as: Hamburg University.

Control of TH17 cells occurs in the small intestine.

Abstract: Interleukin (IL)-17-producing T helper cells (T(H)17) are a recently identified CD4(+) T cell subset distinct from T helper type 1 (T(H)1) and T helper type 2 (T(H)2) cells. T(H)17 cells can drive antigen-specific autoimmune diseases and are considered the main population of pathogenic T cells driving experimental autoimmune encephalomyelitis (EAE), the mouse model for multiple sclerosis. The factors that are needed for the generation of T(H)17 cells have been well characterized. However, where and how the immune system controls T(H)17 cells in vivo remains unclear. Here, by using a model of tolerance induced by CD3-specific antibody, a model of sepsis and influenza A viral infection (H1N1), we show that pro-inflammatory T(H)17 cells can be redirected to and controlled in the small intestine. T(H)17-specific IL-17A secretion induced expression of the chemokine CCL20 in the small intestine, facilitating the migration of these cells specifically to the small intestine via the CCR6/CCL20 axis. Moreover, we found that T(H)17 cells are controlled by two different mechanisms in the small intestine: first, they are eliminated via the intestinal lumen; second, pro-inflammatory T(H)17 cells simultaneously acquire a regulatory phenotype with in vitro and in vivo immune-suppressive properties (rT(H)17). These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells.

Glioma invasion in the central nervous system.

Abstract: Invading glioma cells seem to follow distinct anatomic structures within the central nervous system. Tumor cell dissemination may occur along structures, such as the basement membranes of blood vessels or the glial limitans externa, that contain extracellular matrix (ECM) proteins. Frequently, invasive glioma cells are also found to migrate along myelinated fiber tracts of white matter. This behavior is most likely a consequence of using constitutive extracellular ligands expressed along the pathways of preferred dissemination. The extracellular space in anatomic structures, such as blood vessel basement membranes or between myelinated axons, is profoundly different, thus suggesting that glioma cells may be able to use a multiplicity of matrix ligands, possibly activating separate mechanisms for invasion. In addition, enzymatic modification of the extracellular space or deposition of ECM by the tumor cells may also create a more permissive environment for tumor spread into the adjacent brain. Tumor cell invasion is defined as translocation of neoplastic cells through host cellular and ECM barriers. This process has been studied in other cancers, in which a cascade of events has been described that involves receptor-mediated matrix adhesion, degradation of matrix by tumor-secreted metalloproteinases, and, subsequently, active cell locomotion into the newly created space. Although some of these mechanisms may play an important role in glioma invasion, there are some significant differences that are mainly the result of the profoundly different composition of the extracellular environment within the brain. This review focuses on the composition of central nervous system ECM and the recent evidence for the use by glioma cells of multiple invasion mechanisms in response to this unique environment.

Performance of CMS muon reconstruction in pp collision events at sqrt(s) = 7 TeV

Abstract: The performance of muon reconstruction, identification, and triggering in CMS has been studied using 40 inverse picobarns of data collected in pp collisions at sqrt(s) = 7 TeV at the LHC in 2010. A few benchmark sets of selection criteria covering a wide range of physics analysis needs have been examined. For all considered selections, the efficiency to reconstruct and identify a muon with a transverse momentum pT larger than a few GeV is above 95% over the whole region of pseudorapidity covered by the CMS muon system, abs(eta)<2.4, while the probability to misidentify a hadron as a muon is well below 1%. The efficiency to trigger on single muons with pT above a few GeV is higher than 90% over the full eta range, and typically substantially better. The overall momentum scale is measured to a precision of 0.2% with muons from Z decays. The transverse momentum resolution varies from 1% to 6% depending on pseudorapidity for muons with pT below 100 GeV and, using cosmic rays, it is shown to be better than 10% in the central region up to pT = 1 TeV. Observed distributions of all quantities are well reproduced by the Monte Carlo simulation.