Programmed cell death of myelin basic protein-specific T lymphocytes is reduced in patients with acute multiple sclerosis

We investigated the apoptosis of myelin basic protein (MBP)-specific T lymphocytes in multiple sclerosis (MS) patients with acute (AMS) or stable (SMS) MS by evaluating the expression of apoptosis markers on peripheral cells. Cells of healthy controls (HC) were evaluated as well. Results showed that...

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Published inJournal of neuroimmunology Vol. 166; no. 1; pp. 173 - 179
Main Authors Saresella, Marina, Marventano, Ivana, Speciale, Livianna, Ruzzante, Stefania, Trabattoni, Daria, Silvia Della Bella, Filippi, Massimo, Fasano, Francesca, Cavarretta, Rosella, Caputo, Domenico, Clerici, Mario, Ferrante, Pasquale
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LanguageEnglish
Published Netherlands Elsevier B.V 01.09.2005
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Abstract We investigated the apoptosis of myelin basic protein (MBP)-specific T lymphocytes in multiple sclerosis (MS) patients with acute (AMS) or stable (SMS) MS by evaluating the expression of apoptosis markers on peripheral cells. Cells of healthy controls (HC) were evaluated as well. Results showed that mitogen-stimulated apoptosis was comparable among patients and controls, whereas MBP-stimulated CD4+ and CD8+ 7-AAD+ and 7-AAD+ Fas+ cell (apoptotic cells) were significantly reduced in AMS patients. A reduction of the apoptotic rate of myelin-specific CD4+ and CD8+ T lymphocytes could be involved in the immune-mediated destruction of the myelin sheath seen in AMS patients.
AbstractList We investigated the apoptosis of myelin basic protein (MBP)-specific T lymphocytes in multiple sclerosis (MS) patients with acute (AMS) or stable (SMS) MS by evaluating the expression of apoptosis markers on peripheral cells. Cells of healthy controls (HC) were evaluated as well. Results showed that mitogen-stimulated apoptosis was comparable among patients and controls, whereas MBP-stimulated CD4+ and CD8+7-AAD+ and 7-AAD+ Fas+ cell (apoptotic cells) were significantly reduced in AMS patients. A reduction of the apoptotic rate of myelin-specific CD4+ and CD8+T lymphocytes could be involved in the immune-mediated destruction of the myelin sheath seen in AMS patients.
We investigated the apoptosis of myelin basic protein (MBP)-specific T lymphocytes in multiple sclerosis (MS) patients with acute (AMS) or stable (SMS) MS by evaluating the expression of apoptosis markers on peripheral cells. Cells of healthy controls (HC) were evaluated as well. Results showed that mitogen-stimulated apoptosis was comparable among patients and controls, whereas MBP-stimulated CD4+ and CD8+ 7-AAD+ and 7-AAD+ Fas+ cell (apoptotic cells) were significantly reduced in AMS patients. A reduction of the apoptotic rate of myelin-specific CD4+ and CD8+ T lymphocytes could be involved in the immune-mediated destruction of the myelin sheath seen in AMS patients.
Author Silvia Della Bella
Saresella, Marina
Speciale, Livianna
Ferrante, Pasquale
Trabattoni, Daria
Filippi, Massimo
Fasano, Francesca
Cavarretta, Rosella
Caputo, Domenico
Ruzzante, Stefania
Clerici, Mario
Marventano, Ivana
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Issue 1
Keywords Multiple sclerosis
Immunology
T lymphocyte
Myelin basic protein
Apoptosis
Language English
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Snippet We investigated the apoptosis of myelin basic protein (MBP)-specific T lymphocytes in multiple sclerosis (MS) patients with acute (AMS) or stable (SMS) MS by...
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SubjectTerms Acute Disease
Adult
Apoptosis
Biomarkers - metabolism
Case-Control Studies
CD4-Positive T-Lymphocytes - drug effects
CD4-Positive T-Lymphocytes - metabolism
fas Receptor - metabolism
Female
Humans
Immunology
Male
Middle Aged
Multiple sclerosis
Multiple Sclerosis - metabolism
Multiple Sclerosis - pathology
Multiple Sclerosis - physiopathology
Myelin basic protein
Myelin Basic Protein - metabolism
Myelin Basic Protein - pharmacology
Proto-Oncogene Proteins c-bcl-2 - metabolism
T lymphocyte
Tetradecanoylphorbol Acetate - pharmacology
Title Programmed cell death of myelin basic protein-specific T lymphocytes is reduced in patients with acute multiple sclerosis
URI https://dx.doi.org/10.1016/j.jneuroim.2005.05.010
https://www.ncbi.nlm.nih.gov/pubmed/16161213
https://search.proquest.com/docview/17349111
Volume 166
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