Report on the 2nd scientific meeting of the "Verein zur Förderung des Wissenschaftlichen Nachwuchses in der Neurologie" (NEUROWIND e.V.) held in Motzen, Germany, Oct. 29'th - Oct. 31'st, 2010.

MEETING REPORT Open Access
Report on the 2nd scientific meeting of the
“Verein zur Förderung des Wissenschaftlichen
Nachwuchses in der Neurologie” (NEUROWIND
e.V.) held in Motzen, Germany, Oct. 29’th - Oct.
31’st, 2010
Tim Magnus1*, Ralf A Linker2*, Sven G Meuth3*, Christoph Kleinschnitz4* and Thomas Korn5*
Summary of the scientific contributions to the
NEUROWIND meeting 2010: Contributions in the
fields of neuroimmunology and
neurodegeneration
T cell driven autoimmune inflammation in the CNS has
widely been investigated in the model of experimental
autoimmune encephalomyelitis (EAE) [1]. During dec-
ades of EAE research, it has been established that auto-
reactive T cells are activated in the peripheral immune
tissue, then enter the CNS compartment and - upon
local re-activation - acquire the ability to invade the
CNS parenchyma and exert effector functions. Only
with the advent of modern imaging techniques has it
become possible to actually visualize the individual steps
of T cell activation in the lymph nodes, of crossing the
blood brain barrier, and of interaction between auto-
reactive T cells and their molecular targets within the
CNS. Alexander Flügel has adapted the model of adop-
tive transfer EAE for imaging purposes making inflam-
matory processes accessible to two-photon-microscopy
in situ. By retroviral expression of fluorescent proteins in
encephalitogenic T cells, these T cells were visualized in
vivo by two photon microscopy [2]. Christian Schläger
from Alexander Flügel’s group showed two-photon scan-
ning data providing evidence that in the CNS vasculature
encephalitogenic T cells tended to crawl against the
blood stream before they left the vessel lumen in order to
enter the perivascular space. Here, the cells appeared to
be scanning their environment and only upon productive
contact with antigen presenting cells that presented the
appropriate antigen, T cells were instructed to infiltrate
into the CNS parenchyma. It is becoming increasingly
clear that many features of leukocyte extravasation in the
CNS vasculature are unique and distinct from leukocyte
extravasation in other vascular territories [3]. The
advanced imaging tools that are now available hold
promise to address current questions of T lymphocyte
biology at the blood brain barrier: Why do lymphocytes
move against the blood stream in the CNS microvascula-
ture? Do lymphocytes trespass the endothelial barrier
in a paracellular or transcellular way? How and to what
extent do T cells become activated in the perivascular
space?
The technology of two-photon-microscopy even allows
monitoring immune cell-target interactions within the
CNS parenchyma. In a recently published study, Volker
Siffrin from the group of Frauke Zipp investigated the
interaction of encephalitogenic CD4+ T cells with neu-
ronal structures in the brain stem in vivo. Interestingly,
myelin antigen reactive (2D2) T cells of the Th17 phe-
notype were able to interact with (and damage) axons.
While IFN-g producing Th1 cells failed to induce neuro-
nal apoptosis, Th17 cells were very efficient in promot-
ing axonal damage. The mechanism of lesion
development has not yet been entirely unraveled. While
the interaction between CD4+ T cells and axons was
independent of the T cell receptor (which in this case
was MOG35-55 specific) and thus not restricted by MHC
class II expression on axons, ICAM-1 expression by
* Correspondence: t.magnus@uke.uni-hamburg.de; ralf.linker@uk-erlangen.de;
sven.meuth@ukmuenster.de; christoph.kleinschnitz@mail.uni-wuerzburg.de;
korn@lrz.tum.de
1Department of Neurology, University Clinic Hamburg-Eppendorf, Martinistr.
52,20246 Hamburg, Germany
2Department of Neurology, Friedrich-Alexander-Universität Erlangen,
Schwabachanlage 6,91054 Erlangen, Germany
Full list of author information is available at the end of the article
Magnus et al. Experimental & Translational Stroke Medicine 2011, 3:3
http://www.etsmjournal.com/content/3/1/3
© 2011 Magnus et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons
Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in
any medium, provided the original work is properly cited.

axons and LFA-1 expression by T cells was critically
required for Th17-axonal interaction. Axons responded
to Th17 cell-mediated attack by Ca2+ influx, which was
partially reversible by blockade of NMDA receptors[4].
Thus, Th17 cells exerted effector functions in the CNS
that appeared to be unique to this effector T cell subset.
In order to test the functional relevance of susceptibil-
ity genes identified in the genome-wide association stu-
dies in MS, it is a promising approach to investigate
whether the expression level of the corresponding gene
products on T cells correlates with an altered functional
phenotype of these cells. Melanie Piedavent from the
group of Manuel Friese analysed the expression of
CD226 on human and mouse CD4+ and CD8+ T cells.
CD226 interacts with its ligand CD155 on antigen pre-
senting cells and has a role as a costimulatory molecule.
The nonsynonymous single nucleotide polymorphism
(SNP) rs763361/Gly307Ser in exon 7 of CD226 leads to
the substitution of serine for glycine in the amino acid
sequence of CD226 and has been associated with
increased risk for type 1 diabetes, MS, rheumatoid
arthritis and autoimmune thyroid disease [5]. Both in
mouse and in human CD4+ T cells, low and high
expression of CD226 segregated with markers of naive
and antigen experienced/memory T cells, respectively.
CD8+ T cells expressed high amounts of CD226 in a
constitutive manner. The functional consequences of
rs763361/Gly307Ser are not known. It is possible that
the amino acid substitution at position 307 alters the
phosphorylation sites of CD226 at positions 322 and
329. Alternatively, an altered expression pattern of
CD226 could be induced. Using a mouse model, the
functional consequences of Gly307Ser can now be tested
in vivo.
The role of gδ T cells in EAE has recently been inves-
tigated in more detail. gδ T cells have drawn attention
since a subset of gδ T cells was identified to be highly
responsive to IL-23, which is known to be a potent dri-
ver of autoimmunity and chronic inflammation. Thus,
the role of gδ T cells in models of autoimmunity has
been revisited. Franziska Petermann from the group of
Thomas Korn could show that gδ T cells that respond
to IL-23 were very efficient in inhibiting Treg responses.
As a result, adaptive immune responses flared up in a
milieu that was enriched in IL-23R+gδ T cells [6]. While
the mechanism of this particular function of gδ T cells
has to be further investigated, the role of IL-23R+gδ
T cells in restraining Treg responses was clinically rele-
vant. Tcrd KO mice that lack gδ T cells had exaggerated
Treg responses. Conversely, deletion of Tregs in Tcrd
KO mice restored full susceptibility to EAE [6].
In addition to T cells, B cells are increasingly recog-
nized as important players in neuroimmunological dis-
eases. This concept is also supported by the therapeutic
efficacy of the B cell depleting anti CD20 antibody
rituxan in neuroimmunological disorders. Miguel
Maurer from the group of Jan Lünemann, Zurich ana-
lyzed the B cell repertoire after rituxan treatment of
anti-myelin associated glycoprotein (MAG) antibody
positive paraproteinemic neuropathy, an autoimmune
disorder of the peripheral nervous system characterized
by the presence of antibodies against myelin associated
glycoprotein MAG. Rituxan did not influence the B cell
receptor repertoire, but reduced clonal expansions of
IgM positive memory B cells with reactivity against
MAG protein.
The EAE model is an excellent model to investigate
T cell development and T cell regulation in vivo. How-
ever, the role of antibodies in autoimmune neuroinflam-
mation is not well addressed in classical MOG35-55
induced EAE. Moreover, since in MS the most relevant
autoantigen is still unknown, the function of EAE as a
model for MS is limited in various aspects. On the
other hand, a considerable body of knowledge has
emerged in the recent years on the target antigen in
neuromyelitis optica (NMO) which has been regarded as
a variant of MS. However, NMO is probably a distinct
disease because the target autoantigen is aquaporin-4
(AQP4) which is not a myelin antigen. AQP4 is a water
channel protein which is expressed in astrocytic endfeet
of the lamina gliae limitans and thus plays an important
part in the function of the blood/brain- and CSF/brain-
barriers [7]. Antibodies to AQP4 (NMO-IgG) have been
identified in sera of NMO patients and were proven to
be a useful biomarker for NMO since NMO-IgG are
negative in MS patients [8,9]. NMO-IgG have now been
included in the diagnostic criteria for NMO [10]. How-
ever, it has still been unclear whether antibodies to
AQP4 that are usually not produced intrathecally are
pathogenetically relevant. Several laboratories have
designed experiments in order to test whether NMO-
IgG was able to induce damage to astrocytes [11-13]. In
one approach, which was presented by Claudia Wrzos
from the group of Christine Stadelmann, a subclinical
EAE was induced in experimental rats by active immu-
nization with MBP72-85 in CFA followed by intravenous
transfer of either control IgG or recombinant monoclo-
nal anti-AQP4 IgG. Recombinant anti-AQP4 antibodies
were engineered from heavy and light chain genes iso-
lated from intrathecal plasma cells of NMO patients.
The heavy and light chain genes were cloned into
human framework cassettes and expressed in HEK293
cells. Recombinant immunoglobulins recognized both
the M1 and M23 translational isoform of AQP4. Only
when rats received anti-AQP4 antibodies, they show
astrocytic damage, Ig deposition, and complement acti-
vation at the blood brain barrier in histopathological
analyses. In a second approach, recombinant anti-AQP4
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antibodies were injected intrathecally together with
human complement. Here, astrocyte loss was detected
as early as 1 h after injection and oligodendrocyte apop-
tosis (NogoA+caspase-3+) as early as 3 h after injection.
These experiments were among the first to suggest that
NMO-IgG might have pathogenic relevance beyond
their great value as biomarker. Thus, astrocytes at the
blood brain barrier appear to be a prime target of the
inflammatory process in NMO.
The blood brain barrier (BBB) can be the primary tar-
get of an autoimmune reaction - as in NMO. However,
the blood brain barrier is also crucial in modulating the
pathogenic process in a series of inflammatory, ischemic,
and degenerative diseases. Therefore, it is essential to
understand the function of the BBB in health and dis-
ease. In the laboratory of Sven Meuth, it was found that
a member of the two-pore domain potassium channel
family (K2P), namely TWIK-related K
+-channel gene
(TREK-1) is expressed on murine and human endothe-
lial cells. Inhibition of channel activity by pharmacologi-
cal strategies or during inflammation was associated
with a decreased transendothelial resistance (TER) in an
in vitro model of the BBB. Activation of channel activity
resulted in increased TER and decreased transmigration
of immune cells in the same model. Translated to an in
vivo model Stefan Bittner demonstrated an enhanced
EAE disease course in TREK-/- mice after MOG35-55
immunization while activation of the channel in vivo
using riluzole and/or a-linolenic acid resulted in a sig-
nificantly ameliorated EAE phenotype with reduced cel-
lular infiltrates.
Dirk Hermann presented data on the regulation of
luminal and abluminal ATP binding cassette transpor-
ters in CNS endothelial cells. ABCB1 is expressed in the
luminal membrane and ABCC1 in the abluminal mem-
brane. Upon ischemia, ABCB1 was up-regulated, while
ABCC1 was down-regulated suggesting that the efflux
of xenobiotics out of ischemic brain regions was facili-
tated while the influx of molecules using the ABC trans-
porter system would be severely inhibited [14].
Interestingly, ApoE mediated the regulation of ABC
transporters in the luminal and abluminal membranes
via ApoE receptor 2 and the deactivation of JNK1/2 by
dephosphorylation. As a consequence, ApoE KO mice
showed decreased expression of ABCB1 and increased
expression of abluminal ABCC1 upon ischemic brain
injury. Thus, modulation of the ABC system appears to
be possible by targeting ApoE which has the role of a
molecular switch. This system could be exploited to
facilitate the delivery of neuroprotective drugs into
ischemic brain regions.
In addition to the investigation of immune cells and
the blood brain barrier, studies on the target cells of the
nervous system have been in the focus of interest in
neuroimmunological research. To investigate the role of
cells of the oligodendrocyte lineage, Karin Hagemeier
from Tanja Kuhlmann`s group in Muenster presented a
new co-culture system with primary oligodendrocyte
precursor cells and retinal ganglion cells allowing for
the analysis of oligodendrocyte - neuron interaction on
a single animal basis with high cell purity. In particular,
a focus of interest has been on factors influencing cell
death of oligodendrocytes. Here, p53 induced pro-apop-
totic member of the Bcl2 family (PUMA) is an interest-
ing candidate and the analysis of PUMA deficient cells
in culture and PUMA deficient mice in the cuprizone
model of de- and remyelination in vivo will reveal the
role of this factor in the regulation of oligodendrocyte
survival.
In order to understand the role of microglial cells in
remyelination, the cuprizone model was also investi-
gated in Martin Stangel’s laboratory. During 6 weeks of
cuprizone feeding, toxic demyelination is induced in the
absence of blood brain barrier breakdown. Remyelina-
tion occurs when cuprizone feeding is stopped and
takes 6 weeks to be completed. Demyelination is pre-
ceded by microglia activation and proliferation by
2 weeks, and remyelination is preceded by proliferation
of oligodendrocyte precursor cells (OPC). Thomas
Skripuletz from Martin Stangel’s laboratory realized that
administration of LPS modulated both de- and remyeli-
nation in the cuprizone model. The net effect of LPS
was beneficial because demyelination was decelerated
and remyelination was enhanced. In histological ana-
lyses, the proliferation of microglial cells seemed to be
inhibited while the proliferation of OPCs was increased
by LPS. Thus, both de- and remyelination are modu-
lated by TLR ligands in an indirect manner. However, it
remains to be determined whether the decreased prolif-
eration of microglia by LPS, which is able to cross the
intact BBB, is the direct cause of decreased demyelina-
tion in this model.
In view of the degenerative changes in autoimmune
demyelination, neuroprotective approaches are of high
interest in MS therapy. De-Hyung Lee from the group
of Ralf Linker, Erlangen, presented data on mechanisms
of action of fumaric acid esters (FAE), which are cur-
rently under investigation as new oral disease modifying
drug in relapsing remitting MS. Application of FAE in
the MOG-EAE model resulted in an ameliorated course
of chronic EAE and a preservation of neurons, oligoden-
drocytes and myelin as well as reduced astrogliosis with-
out direct influence on the immune reaction. These
neuroprotective effects were associated with the activa-
tion of nuclear factor (erythroid-derived 2)-like 2 (Nrf2),
a transcription factor involved in the cellular detoxifica-
tion pathways and the natural antioxidative response
[15].
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Finally, degenerative processes in autoimmune demye-
lination share several features with primary neurodegen-
erative diseases like amyotrophic lateral sclerosis (ALS)
or Alzheimer’s disease (AD). Sarah Kaiser from the
Department of Neurology, University Hospital Ulm, pre-
sented data on several cerebrospinal fluid (CSF) biomar-
kers in ALS. The group of Johannes Brettschneider
could show that SMI 35 (representing heavy neurofila-
ments) was increased in rapidly progressing ALS. In
contrast, CSF levels of soluble amyloid precursor protein
(sAPP) did not show differences to controls, but nega-
tively correlated with disease duration. In conclusion,
the NFH/sAPP ratio may represent a new biomarker for
ALS progression and may also be of interest in diseases
like MS.
The intimate mechanistic relationship between neuro-
degenerative and neuroinflammatory disease processes is
further highlighted by the immune reaction in AD
which particularly involves microglial activation. Here,
Marius Krauthausen from the group of Marcus Mueller,
Bonn, gave an update on their studies on chemokines in
the transgenic APP/PS1 model of AD. They investigated
the role of CXCR3 in a genetic approach by crossing
APP/PS1 mice with CXCR3-deficient mice. As com-
pared to APP/PS1 transgenic controls, these mice dis-
play a reduced plaque burden and reduced Ab protein
load associated with a reduced activation and accumula-
tion of periplaque microglia. These data argue for a role
of chemokines in plaque formation which may be criti-
cally modulated by the function of microglia.
So far, therapeutic options in neurodegenerative dis-
eases are limited. Recently, the application of small inhi-
bitory RNA (siRNA) came into the focus of interest.
Anderson de Andrade and Xu Hong, both from Guenter
Hoeglinger’s group in Marburg, employed siRNA as new
therapeutic approach in tauopathies and synucleinopa-
thies. In vitro models using adenoviral overexpression of
alpha synuclein in dopaminergic neurons and the in
vivo model of P301S tau transgenic mice will allow for
refined protocols of siRNA application and thus testing
the effect of synuclein or tau knock-down as new thera-
peutic approaches in neurodegenerative diseases.
Contributions on stroke and vascular pathology
In the stroke field, the role of the immune system was
discussed. First studies show that specific inhibition of
sphingolipid signaling or inhibition of adhesion mole-
cules can be beneficial. Waltraud Pfeilschifter from
Frankfurt presented data that treatment with FTY720, a
functional sphingosin 1 phosphate receptor 1 antagonist
which blocks the egress of lymphocytes from the lymph
node, reduced ischemic damage in the middle cerebral
artery occlusion (MCAO) model. It also reduced the
activation of the immune system and apoptotic cell
death. Arthur Liesz from Heidelberg demonstrated the
potential of interfering with the migration of leucocytes
across the blood brain barrier by inhibition of VCAM
through antibody or siRNA[16]. Especially, the gene
silencing resulted in a better outcome in the MCAO
model. Furthermore, Friederike Vollmar from the group
of Christoph Kleinschnitz in Wuerzburg highlighted
novel findings on the role of the proinflammatory kallik-
rein-kinin-system (KKS) in the pathophysiology of acute
ischemic stroke. As previously shown, depletion or phar-
macological blockade of the bradykinin receptor B1
(B1R), but not B2R, attenuated postischemic inflamma-
tion and blood-brain-barrier damage both after transient
middle cerebral artery occlusion or traumatic brain
injury in mice [17,18]. In a follow-up project, the group
currently investigates whether additional molecules
located upstream of the kinin receptors such as kinino-
gen or plasma kallikrein are likewise involved in stroke-
induced inflammation and neuronal damage. Preliminary
data obtained in kininogen(kng)-deficient mice were indi-
cative for a potential role of KNG for thrombus forma-
tion and edema formation in the ischemic brain.
However, the immune regulation in stroke is quite
complex and involves different subclasses of immune
cells. Mathias Gelderblom from the group of Tim Mag-
nus showed that three days following stroke gδ T cells
emerged in the ischemic hemisphere. The majority of gδ
T cells were located in direct proximity to the infarct
core. 40% of these atypical T cells produced IL 17A and
seemed to have a role in recruiting neutrophils to the
area of destruction. The complexity of the immunologic
reperfusion response after stroke and possible pitfalls in
immune cell depletion approaches as a potential thera-
peutic strategy were further underscored by the observa-
tion of Michael Gliem from Sebastian Jander’s group
showing that depletion of macrophages with clodronate
resulted in an increased bleeding rate after MCAO.
The peptide hormone Ghrelin is known as the ligand
of the growth hormone secretagogue receptor. Ghrelin
crosses the blood-brain barrier and binds to hippocam-
pal neurons thereby promoting dendritic spine synapse
formation and proliferation of progenitor cells. Kai
Diederich together with Jens Minnerup from Münster
demonstrated that Ghrelin treatment improves func-
tional recovery after photothrombotic stroke in rats
probably by enhancing the generation of newborn
hippocampal neurons.
Felix Schlachetzki from Regensburg reviewed basic
mechanisms of blood-brain barrier (BBB) damage fol-
lowing brain ischemia/reperfusion injury which is asso-
ciated with intracerebral hemorrhage and edema
formation. He pointed out that in experimental stroke
BBB permeability is bi-phasic for certain contrast agents
(para-endothelial efflux) yet vasogenic edema is a
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monophasic event (trans-endothelial efflux) as shown by
serial post-contrast MRI and T2-relaxometry. However,
the bi-phasic BBB response may be linked to both dele-
terious and regenerative effects at the neurovasular unit
[19].
In conclusion, by bringing together researchers in the
fields of neuroimmunology, neurodegeneration, and
neurovascular diseases, this meeting has again been a
valuable platform to discuss pathogenic cascades com-
mon to these different disorders. Access of immune
cells (innate or adaptive) to different body compart-
ments and in particular to the CNS are clearly common
themes in a variety of neurological diseases. It is our
hope that the NEUROWIND meeting will teach us how
it might be possible to advance the understanding of
pathogenic processes in neurological disorders by
exchanging concepts and tools between various CNS
disease models.
Acknowledgements
The NEUROWIND e.V. scientific meeting was kindly supported by Merck
Serono GmbH, Darmstadt, Germany (unrestricted grant to NEUROWIND e.V.).
We thank Ms. Anke Bauer, Würzburg, and Patrick Meuth, Münster, for editing
the manuscript. This publication was funded by the German Research
Foundation (DFG) in the funding programme Open Access Publishing.
List of speakers at the second scientific meeting of NEUROWIND e.V.
(in alphabetical order)
Anderson de Andrade, Dept. of Neurology, University of Marburg, Germany
Stefan Bittner, Dept. of Neurology, University of Münster, Germany
Kai Diederich, Dept. of Neurology, University of Münster, Germany
Ulrich Dirnagl, Dept. of Neurology and Experimental Neurology and Center
for Stroke Research, Berlin Charité University Medicine, Germany
Mathias Gelderblom, Center for Molecular Neurobiology, Hamburg, Germany
Michael Gliem, Dept. of Neurology, University of Düsseldorf, Germany
Karin Hagemeier, Dept. of Neurology, University of Münster, Germany
Dirk Hermann, Dept. of Neurology, University of Essen, Germany
Sarah Kaiser, Dept. of Neurology, University of Ulm, Germany
Marius Krauthausen, Dept. of Neurology, University of Bonn, Germany
De-Hyung Lee, Dept. of Neurology, University of Bochum, Germany
Arthur Liesz, Dept. of Neurology, University of Heidelberg, Germany
Miguel Maurer, Institute for Experimental Neurology, University of Zürich,
Switzerland
Philipp Mergenthaler, Charité University Medicine, Berlin, Germany
Franziska Petermann, Dept. of Neurology, Technical University of Munich,
Germany
Waltraud Pfeilschifter, Dept. of Neurology, University of Frankfurt, Germany
Melanie Piedavent, Center for Molecular Neurobiology, Hamburg, Germany
Franziska Scheibe, Dept. of Experimental Neurology, Berlin Charité University
Medicine, Germany
Felix Schlachetzki, Dept. of Neurology, University Regensburg, Germany
Christian Schläger, Dept. of Neuroimmunology, Institute for MS Research,
Göttingen, Germany
Thomas Skripuletz, Hannover Medical School, Germany
Volker Siffrin, Dept. of Neurology, University of Mainz, Germany
Friederike Vollmar, Dept. of Neurology, University of Würzburg, Germany
Claudia Wrzos, Dept. of Neurology, University of Göttingen, Germany
Hong Xu, Marburg, Dept. of Neurology, University of Marburg, Germany
Author details
1Department of Neurology, University Clinic Hamburg-Eppendorf, Martinistr.
52,20246 Hamburg, Germany. 2Department of Neurology, Friedrich-
Alexander-Universität Erlangen, Schwabachanlage 6,91054 Erlangen,
Germany. 3Department of Neurology-Inflammatory Disorders of the Nervous
System and Neuro-oncology, Westfälische Wilhelms-University Münster,
Domagkstr. 13,48149 Münster, Germany. 4Department of Neurology, Julius-
Maximilians University of Würzburg, Josef-Schneider-Str. 11,97080 Würzburg,
Germany. 5Department of Neurology, Klinikum rechts der Isar, Technical
University Munich, Ismaninger Str. 22,81675 Munich, Germany.
Authors’ contributions
TM, RL, SGM, CK, and TK wrote the paper. All authors read and approved the
final manuscript.
Competing interests
The authors declare that they have no competing interests.
Received: 23 March 2011 Accepted: 1 April 2011 Published: 1 April 2011
References
1. Korn T, Mitsdoerffer M, Kuchroo VK: Immunological basis for the
development of tissue inflammation and organ-specific autoimmunity in
animal models of multiple sclerosis. Results and Problems in Cell
Differentiation 2010, 51:43-74.
2. Flugel A, Berkowicz T, Ritter T, Labeur M, Jenne DE, Z Li, Ellwart JW,
Willem M, Lassmann H, Wekerle H: Migratory activity and functional
changes of green fluorescent effector cells before and during
experimental autoimmune encephalomyelitis. Immunity 2001, 14:547-560.
3. Bartholomaus I, Kawakami N, Odoardi F, Schlager C, Miljkovic D, Ellwart JW,
Klinkert WE, Flugel-Koch C, Issekutz TB, Wekerle H, Flugel A: Effector T cell
interactions with meningeal vascular structures in nascent autoimmune
CNS lesions. Nature 2009, 462:94-98.
4. Siffrin V, Radbruch H, Glumm R, Niesner R, Paterka M, Herz J, Leuenberger T,
Lehmann SM, Luenstedt S, Rinnenthal JL, Laube G, Luche H, Lehnardt S,
Fehling HJ, Griesbeck O, Zipp F: In vivo imaging of partially reversible
th17 cell-induced neuronal dysfunction in the course of
encephalomyelitis. Immunity 2010, 33:424-436.
5. Hafler JP, Maier LM, Cooper JD, Plagnol V, Hinks A, Simmonds MJ,
Stevens HE, Walker NM, Healy B, Howson JM, Maisuria M, Duley S,
Coleman G, Gough SC, Worthington J, Kuchroo VK, Wicker LS, Todd JA:
CD226 Gly307Ser association with multiple autoimmune diseases. Genes
Immun 2009, 10:5-10.
6. Petermann F, Rothhammer V, Claussen MC, Haas JD, Blanco LR, Heink S,
Prinz I, Hemmer B, Kuchroo VK, Oukka M, Korn T: gammadelta T cells
enhance autoimmunity by restraining regulatory T cell responses via an
interleukin-23-dependent mechanism. Immunity 2010, 33:351-363.
7. Verkman AS: Aquaporins: translating bench research to human disease.
Journal of Experimental Biology 2009, 212:1707-1715.
8. Lennon VA, Wingerchuk DM, Kryzer TJ, Pittock SJ, Lucchinetti CF, Fujihara K,
Nakashima I, Weinshenker BG: A serum autoantibody marker of
neuromyelitis optica: distinction from multiple sclerosis. Lancet 2004,
364:2106-2112.
9. Kalluri SR, Illes Z, Srivastava R, Cree B, Menge T, Bennett JL, Berthele A,
Hemmer B: Quantification and functional characterization of antibodies
to native aquaporin 4 in neuromyelitis optica. Archives of Neurology 2010,
67:1201-1208.
10. Wingerchuk DM, Lennon VA, Pittock SJ, Lucchinetti CF, Weinshenker BG:
Revised diagnostic criteria for neuromyelitis optica. Neurology 2006,
66:1485-1489.
11. Bradl M, Misu T, Takahashi T, Watanabe M, Mader S, Reindl M,
Adzemovic M, Bauer J, Berger T, Fujihara K, Itoyama Y, Lassmann H:
Neuromyelitis optica: pathogenicity of patient immunoglobulin in vivo.
Annals of Neurology 2009, 66:630-643.
12. Bennett JL, Lam C, Kalluri SR, Saikali P, Bautista K, Dupree C, Glogowska M,
Case D, Antel JP, Owens GP, Gilden D, Nessler S, Stadelmann C, Hemmer B:
Intrathecal pathogenic anti-aquaporin-4 antibodies in early
neuromyelitis optica. Annals of Neurology 2009, 66:617-629.
13. Saadoun S, Waters P, Bell BA, Vincent A, Verkman AS, Papadopoulos MC:
Intra-cerebral injection of neuromyelitis optica immunoglobulin G and
human complement produces neuromyelitis optica lesions in mice. Brain
2010, 133:349-361.
14. ElAli A, Hermann DM: Apolipoprotein E controls ATP-binding cassette
transporters in the ischemic brain. Sci Signal 2010, 3:ra72.
15. Linker RA, Lee DH, Ryan S, van Dam AM, Conrad R, Bista P, Zeng W,
Hronowsky X, Buko A, Chollate S, Ellrichmann G, Bruck W, Dawson K,
Magnus et al. Experimental & Translational Stroke Medicine 2011, 3:3
http://www.etsmjournal.com/content/3/1/3
Page 5 of 6