FN Thomson Reuters Web of Knowledge
VR 1.0
PT J
AU Kleindienst, T
   Winnubst, J
   Roth-Alpermann, C
   Bonhoeffer, T
   Lohmann, C
AF Kleindienst, Thomas
   Winnubst, Johan
   Roth-Alpermann, Claudia
   Bonhoeffer, Tobias
   Lohmann, Christian
TI Activity-Dependent Clustering of Functional Synaptic Inputs on
   Developing Hippocampal Dendrites
SO NEURON
LA English
DT Article
ID NEONATAL-RAT HIPPOCAMPUS; CA1 PYRAMIDAL NEURONS; IN-VIVO; CALCIUM
   TRANSIENTS; SYNAPSES; CELLS; MECHANISMS; PLASTICITY; DYNAMICS; SYSTEM
AB During brain development, before sensory systems become functional,
   neuronal networks spontaneously generate repetitive bursts of neuronal
   activity, which are typically synchronized across many neurons. Such
   activity patterns have been described on the level of networks and
   cells, but the fine-structure of inputs received by an individual neuron
   during spontaneous network activity has not been studied. Here, we used
   calcium imaging to record activity at many synapses of hippocampal
   pyramidal neurons simultaneously to establish the activity patterns in
   the majority of synapses of an entire cell. Analysis of the
   spatiotemporal patterns of synaptic activity revealed a fine-scale
   connectivity rule: neighboring synapses (<16 mu m intersynapse distance)
   are more likely to be coactive than synapses that are farther away from
   each other. Blocking spiking activity or NMDA receptor activation
   revealed that the clustering of synaptic inputs required neuronal
   activity, demonstrating a role of developmentally expressed spontaneous
   activity for connecting neurons with subcellular precision.
C1 [Kleindienst, Thomas; Winnubst, Johan; Lohmann, Christian] Netherlands Inst Neurosci, NL-1105 BA Amsterdam, Netherlands.
   [Kleindienst, Thomas; Roth-Alpermann, Claudia; Bonhoeffer, Tobias; Lohmann, Christian] Max Planck Inst Neurobiol, D-82152 Martinsried, Germany.
RP Lohmann, C (reprint author), Netherlands Inst Neurosci, NL-1105 BA Amsterdam, Netherlands
EM c.lohmann@nin.knaw.nl
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD DEC 22
PY 2011
VL 72
IS 6
BP 1012
EP 1024
DI 10.1016/j.neuron.2011.10.015
PG 13
GA 871XM
UT WOS:000298771000015
ER
PT J
AU Berer, K
   Mues, M
   Koutrolos, M
   Al Rasbi, Z
   Boziki, M
   Johner, C
   Wekerle, H
   Krishnamoorthy, G
AF Berer, Kerstin
   Mues, Marsilius
   Koutrolos, Michail
   Al Rasbi, Zakeya
   Boziki, Marina
   Johner, Caroline
   Wekerle, Hartmut
   Krishnamoorthy, Gurumoorthy
TI Commensal microbiota and myelin autoantigen cooperate to trigger
   autoimmune demyelination
SO NATURE
LA English
DT Article
ID T-CELL RESPONSES; MULTIPLE-SCLEROSIS; B-CELLS; TRANSGENIC MICE;
   AUTOANTIBODIES; INDUCTION; BACTERIA; DISEASE; MOG
AB Active multiple sclerosis lesions show inflammatory changes suggestive
   of a combined attack by autoreactive T and B lymphocytes against brain
   white matter(1). These pathogenic immune cells derive from progenitors
   that are normal, innocuous components of the healthy immune repertoire
   but become autoaggressive upon pathological activation. The stimuli
   triggering this autoimmune conversion have been commonly attributed to
   environmental factors, in particular microbial infection(2). However,
   using the relapsing-remitting mouse model of spontaneously developing
   experimental autoimmune encephalomyelitis(3), here we show that the
   commensal gut flora-in the absence of pathogenic agents-is essential in
   triggering immune processes, leading to a relapsing-remitting autoimmune
   disease driven by myelin-specific CD4(+) T cells. We show further that
   recruitment and activation of autoantibody-producing B cells from the
   endogenous immune repertoire depends on availability of the target
   autoantigen, myelin oligodendrocyte glycoprotein (MOG), and commensal
   microbiota. Our observations identify a sequence of events triggering
   organ-specific autoimmune disease and these processes may offer novel
   therapeutic targets.
C1 [Berer, Kerstin; Mues, Marsilius; Koutrolos, Michail; Al Rasbi, Zakeya; Boziki, Marina; Wekerle, Hartmut; Krishnamoorthy, Gurumoorthy] Max Planck Inst Neurobiol, Dept Neuroimmunol, D-82152 Martinsried, Germany.
   [Johner, Caroline] Max Planck Inst Immunobiol & Epigenet, D-79108 Freiburg, Germany.
RP Wekerle, H (reprint author), Max Planck Inst Neurobiol, Dept Neuroimmunol, D-82152 Martinsried, Germany
EM hwekerle@neuro.mpg.de
   guru@neuro.mpg.de
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 24
PY 2011
VL 479
IS 7374
BP 538
EP U266
DI 10.1038/nature10554
PG 5
GA 851QI
UT WOS:000297285600053
ER
PT J
AU Yamagishi, S
   Hampel, F
   Hata, K
   del Toro, D
   Schwark, M
   Kvachnina, E
   Bastmeyer, M
   Yamashita, T
   Tarabykin, V
   Klein, R
   Egea, J
AF Yamagishi, Satoru
   Hampel, Falko
   Hata, Katsuhiko
   del Toro, Daniel
   Schwark, Manuela
   Kvachnina, Elena
   Bastmeyer, Martin
   Yamashita, Toshihide
   Tarabykin, Victor
   Klein, Ruediger
   Egea, Joaquim
TI FLRT2 and FLRT3 act as repulsive guidance cues for Unc5-positive neurons
RID C-6147-2008
SO EMBO JOURNAL
LA English
DT Article
DE cell migration; cortex development; FLRT; repulsive guidance; Unc5
ID CELL-ADHESION; SUBVENTRICULAR ZONE; NEURITE OUTGROWTH; RECEPTOR GENE;
   AXON GUIDANCE; MIGRATION; MOLECULE; PROTEIN; IDENTIFICATION;
   SPECIFICATION
AB Netrin-1 induces repulsive axon guidance by binding to the mammalian
   Unc5 receptor family (Unc5A-Unc5D). Mouse genetic analysis of selected
   members of the Unc5 family, however, revealed essential functions
   independent of Netrin-1, suggesting the presence of other ligands. Unc5B
   was recently shown to bind fibronectin and leucine-rich transmembrane
   protein-3 (FLRT3), although the relevance of this interaction for
   nervous system development remained unclear. Here, we show that the
   related Unc5D receptor binds specifically to another FLRT protein,
   FLRT2. During development, FLRT2/3 ectodomains (ECDs) are shed from
   neurons and act as repulsive guidance molecules for axons and somata of
   Unc5-positive neurons. In the developing mammalian neocortex, Unc5D is
   expressed by neurons in the sub-ventricular zone (SVZ), which display
   delayed migration to the FLRT2-expressing cortical plate (CP). Deletion
   of either FLRT2 or Unc5D causes a subset of SVZ-derived neurons to
   prematurely migrate towards the CP, whereas overexpression of Unc5D has
   opposite effects. Hence, the shed FLRT2 and FLRT3 ECDs represent a novel
   family of chemorepellents for Unc5-positive neurons and FLRT2/Unc5D
   signalling modulates cortical neuron migration. The EMBO Journal ( 2011)
   30, 2920-2933. doi:10.1038/emboj.2011.189; Published online 14 June 2011
C1 [Yamagishi, Satoru; Hampel, Falko; del Toro, Daniel; Klein, Ruediger; Egea, Joaquim] Max Planck Inst Neurobiol, Dept Mol Neurobiol, D-82152 Martinsried, Germany.
   [Hata, Katsuhiko; Yamashita, Toshihide] Osaka Univ, Grad Sch Med, Dept Mol Neurosci, Osaka, Japan.
   [Schwark, Manuela; Kvachnina, Elena; Tarabykin, Victor] Max Planck Inst Expt Med, D-3400 Gottingen, Germany.
   [Schwark, Manuela; Tarabykin, Victor] Charite, Inst Cell Biol & Neurobiol, D-13353 Berlin, Germany.
   [Bastmeyer, Martin] KIT, Inst Zool, Abt Zell & Neurobiol, Karlsruhe, Germany.
   [Egea, Joaquim] Univ Lleida, IRBLLEIDA, Fac Med, Dept Ciencies Med Basiques, Lleida 25198, Spain.
RP Klein, R (reprint author), Max Planck Inst Neurobiol, Dept Mol Neurobiol, Klopferspitz 18, D-82152 Martinsried, Germany
EM rklein@neuro.mpg.de
   joaquim.egea@cmb.udl.es
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0261-4189
J9 EMBO J
JI Embo J.
PD JUL 20
PY 2011
VL 30
IS 14
BP 2920
EP 2933
DI 10.1038/emboj.2011.189
PG 14
GA 808HZ
UT WOS:000293970100017
ER
PT J
AU Schuster, FR
   Hubner, B
   Fuhrer, M
   Eckermann, O
   Gombert, M
   Dornmair, K
   Binder, V
   Reuther, S
   Krell, P
   Keller, T
   Borkhardt, A
AF Schuster, F. R.
   Hubner, B.
   Fuehrer, M.
   Eckermann, O.
   Gombert, M.
   Dornmair, K.
   Binder, V.
   Reuther, S.
   Krell, P.
   Keller, T.
   Borkhardt, A.
TI Highly skewed T-cell receptor V-beta chain repertoire in the bone marrow
   is associated with response to immunosuppressive drug therapy in
   children with very severe aplastic anemia
SO BLOOD CANCER JOURNAL
LA English
DT Article
DE aplastic anemia; T-cell receptor V-beta chain repertoire; children
ID IMMUNE-RESPONSES; PATHOPHYSIOLOGY; RECONSTITUTION; SURVIVAL; DISEASE
AB One of the major obstacles of immunosuppressive therapy (IST) in
   children with severe aplastic anemia (SAA) comes from the often
   months-long unpredictability of bone-marrow (BM) recovery. In this
   prospective study in children with newly diagnosed very severe AA (n =
   10), who were enrolled in the therapy study SAA-BFM 94, we found a
   dramatically reduced diversity of both CD4+ and CD8+ BM cells, as scored
   by comprehensive V-beta chain T-cell receptor (TCR) analysis. Strongly
   skewed TCR V-beta pattern was highly predictive for good or at least
   partial treatment response (n = 6, CD8+ complexity scoring median 35.5,
   range 24-73). In contrast, IST in patients with rather moderate
   reduction of TCR V-beta diversity (n = 4, CD8+ complexity scoring median
   109.5, range 82-124) always failed (P = 0.0095). If confirmed in a
   larger series of patients, TCR V-beta repertoire in BM may help to
   assign children with SAA up-front either to IST or to allogeneic
   stem-cell transplantation. Blood Cancer Journal (2011) 1, e8;
   doi:10.1038/bcj.2011.6; published online 4 March 2011
C1 [Borkhardt, A.] Univ Dusseldorf, Dept Pediat Oncol Hematol & Clin Immunol, Ctr Child & Adolescent Hlth, Clin Pediat Oncol Hematol & Clin Immunol,Med Fac, D-40225 Dusseldorf, Germany.
   [Fuehrer, M.] Univ Munich, Dept Pediat Oncol & Hematol, Dr von Haunersches Childrens Hosp, Munich, Germany.
   [Dornmair, K.] Univ Munich, Dept Clin Neuroimmunol, Munich, Germany.
   [Keller, T.] Stat Anal GmbH, Acomed, Leipzig, Germany.
RP Borkhardt, A (reprint author), Univ Dusseldorf, Dept Pediat Oncol Hematol & Clin Immunol, Ctr Child & Adolescent Hlth, Clin Pediat Oncol Hematol & Clin Immunol,Med Fac, Moorenstr 5, D-40225 Dusseldorf, Germany
EM arndt.borkhardt@med.uni-duesseldorf.de
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2044-5385
J9 BLOOD CANCER J
JI Blood Cancer J.
PD MAR
PY 2011
VL 1
AR e8
DI 10.1038/bcj.2011.6
PG 4
GA 872NC
UT WOS:000298815400002
ER
PT J
AU Junker, A
   Hohlfeld, R
   Meinl, E
AF Junker, Andreas
   Hohlfeld, Reinhard
   Meinl, Edgar
TI The emerging role of microRNAs in multiple sclerosis
SO NATURE REVIEWS NEUROLOGY
LA English
DT Article
ID OLIGODENDROCYTE DIFFERENTIATION; IN-VIVO; LESIONS; CELLS; SYSTEM; MIRNA;
   IDENTIFICATION; MYELINATION; TARGETS; CD47
AB Several hundred microRNAs (miRNAs) fine-tune the expression of
   approximately half of all human genes. Recent studies have revealed that
   miRNA profiles in blood cells become altered in multiple sclerosis (MS),
   and that active and inactive MS lesions have distinct miRNA expression
   patterns. The dysregulated miRNAs in MS lesions seem to be associated
   with astrocytes and infiltrating immune cells, and might unleash local
   macrophages through downregulation of the self-recognition signal CD47.
   The expression of miRNA-326 in blood cells has been reported to increase
   during relapses. This miRNA promotes T helper 17 cell differentiation
   and is highly abundant in active MS lesions. miRNAs are needed for
   maintenance of the myelin sheath, and the absence of such molecules
   results in axonal damage in mice. miRNA-219 and other miRNAs promote
   oligodendrocyte differentiation. Here, we discuss the possible
   contribution of miRNAs to MS pathogenesis. An improved understanding of
   this contribution should help to identify novel therapeutic targets and
   biomarkers for this disease.
C1 [Hohlfeld, Reinhard; Meinl, Edgar] Univ Munich, Inst Clin Neuroimmunol, D-81377 Munich, Germany.
   [Junker, Andreas] Univ Gottingen, Dept Neuropathol, Univ Med Ctr, D-37075 Gottingen, Germany.
RP Meinl, E (reprint author), Univ Munich, Inst Clin Neuroimmunol, Marchioninistr 15, D-81377 Munich, Germany
EM meinl@neuro.mpg.de
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4758
J9 NAT REV NEUROL
JI Nat. Rev. Neurol.
PD JAN
PY 2011
VL 7
IS 1
BP 56
EP 59
DI 10.1038/nrneurol.2010.179
PG 4
GA 705AG
UT WOS:000286099300012
ER
EF