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#Post#: 1163--------------------------------------------------
(Abst.) Fatal rebound MS activity after Tysabri withdrawal...
By: agate Date: April 3, 2016, 9:31 pm
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From PubMed, April 3, 2016:
[quote]Mult Scler. 2016 Apr 1.
Immunological and pathological characterization of fatal rebound
MS activity following natalizumab withdrawal
Larochelle C1, Metz I2, Lécuyer MA3, Terouz S3, Roger M4, Arbour
N5, Brück W2, Prat A6.
Author information
1Neuroimmunology Research Laboratory, Centre de Recherche du
Centre Hospitalier de l'Université de Montréal (CRCHUM),
Montréal, QC, Canada/Multiple Sclerosis Clinic, Division of
Neurology, CHUM-Notre-Dame Hospital, Montréal, QC,
Canada/Department of Neurosciences, Faculty of Medicine,
Université de Montréal, Montréal, QC, Canada.
2Department of Neuropathology, Faculty of Medicine,
Universitätsmedizin Göttingen, Göttingen, Germany.
3Neuroimmunology Research Laboratory, Centre de Recherche du
Centre Hospitalier de l'Université de Montréal (CRCHUM),
Montréal, QC, Canada.
4Department of Microbiology and Immunology, Faculty of Medicine,
Université de Montréal, Montréal, QC, Canada.
5Neuroimmunology Research Laboratory, Centre de Recherche du
Centre Hospitalier de l'Université de Montréal (CRCHUM),
Montréal, QC, Canada/Department of Neurosciences, Faculty of
Medicine, Université de Montréal, Montréal, QC, Canada.
6Neuroimmunology Research Laboratory, Centre de Recherche du
Centre Hospitalier de l'Université de Montréal (CRCHUM),
Montréal, QC, Canada/Multiple Sclerosis Clinic, Division of
Neurology, CHUM-Notre-Dame Hospital, Montréal, QC,
Canada/Department of Neurosciences, Faculty of Medicine,
Université de Montréal, Montréal, QC, Canada
a.prat@umontreal.ca.
BACKGROUND:
Severe rebound multiple sclerosis (MS) activity is a
life-threatening complication of natalizumab (NTZ) withdrawal,
for which pathogenesis and treatment are still unclear. We
report the immunological and pathological characterization of a
case of central nervous system (CNS) inflammatory demyelination
after NTZ discontinuation.
OBJECTIVE:
To understand the pathophysiology of this neuroinflammatory
condition.
METHODS:
Antemortem blood and cerebrospinal fluid (CSF) analysis was
compared with postmortem pathological studies, as well as with
novel flow cytometry characterization of immune cells isolated
from the CNS parenchyma.
RESULTS:
Pathological analysis of the brain revealed the presence of
innumerable active inflammatory demyelinating lesions typical of
immunopathological pattern II.
Monocytes/macrophages and B cells were enriched in the CNS
parenchyma compared to the CSF. Numerous plasma cells were
present in the lesions, but CD8 T lymphocytes were predominant
in the parenchyma, as opposed to CD4 in the CSF.
CNS-infiltrating lymphocytes expressed high levels of adhesion
molecules, granzyme B (GzB), interferon-gamma (IFN-γ), and
interleukin (IL)-17.
CONCLUSIONS:
Our results underline the differences in immune cell populations
between the CSF and the CNS parenchyma, and suggest that
aggressive immunosuppressive therapy targeting both T and B
lymphocytes is warranted to control the overwhelming CNS
inflammation.[/quote]
The abstract can be seen here
HTML http://www.ncbi.nlm.nih.gov/pubmed/27037182.
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