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#Post#: 1163--------------------------------------------------
(Abst.) Fatal rebound MS activity after Tysabri withdrawal...
DIR 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.
--- End Quote ---
The abstract can be seen here
HTML http://www.ncbi.nlm.nih.gov/pubmed/27037182.
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