URI:
   DIR Return Create A Forum - Home
       ---------------------------------------------------------
       MS Speaks
  HTML https://msspeaks.createaforum.com
       ---------------------------------------------------------
       *****************************************************
   DIR Return to: TYSABRI (natalizumab)
       *****************************************************
       #Post#: 1163--------------------------------------------------
       (Abst.) Fatal rebound MS activity after Tysabri withdrawal...
   DIR By: agate
       Date: April 3, 2016, 9:31 pm
       ---------------------------------------------------------
       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.
       *****************************************************
       Page 1 of 1