Myelin basic protein in CSF as indicator of disease activity in multiple sclerosis

1998 ◽  
Vol 4 (3) ◽  
pp. 124-126 ◽  
Author(s):  
K JB Lamers ◽  
H PM de Reus ◽  
P JH Jongen
Keyword(s):  
Multiple Sclerosis ◽  
Disease Activity ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
Normal Values ◽  
Disease Process ◽  
Intravenous Methylprednisolone ◽  
Relapsing Remitting ◽  
Methylprednisolone Treatment ◽  
Edss Score

There is an evident need for a quantitative laboratory marker for ascertaining disease activity and treatment effects in multiple sclerosis (MS) patients. Activity of the disease process in MS is accompanied by myelin breakdown and appearance of myelin basic protein (MBP) in cerebrospinal fluid (CSF). In this paper MBP in CSF of relapsing-remitting (RR) MS patients is reviewed. MBP in CSF is a fragment containing an epitope corresponding to aminoacid residues 45-89 of the native molecule. From several relevant studies about CSF MBP in RR MS the following relations can be concluded: CSF MBP levels in active MS patients are frequently increased (45-100%), remain increased until 5 to 6 weeks after onset symptoms and are higher in polysymptomatic exacerbations and correlate with number of gadolinium-enhanced (Gd) lesions on MRI, severity of relapses, EDSS score and CSF intrathecal IgM synthesis. After an intravenous methylprednisolone treatment the increased CSF MBP levels return to normal values and reduction in CSF MBP is related to reduction in EDSS score, number of Gd lesions and CSF intrathecal IgM synthesis.

scholarly journals T helper cell type 1 (Th1), Th2 and Th17 responses to myelin basic protein and disease activity in multiple sclerosis

Immunology ◽  
2008 ◽  
Vol 125 (2) ◽  
pp. 161-169 ◽  
Author(s):  
Chris J. Hedegaard ◽  
Martin Krakauer ◽  
Klaus Bendtzen ◽  
Henrik Lund ◽  
Finn Sellebjerg ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Disease Activity ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
T Helper Cell ◽  
Helper Cell ◽  
Cell Type ◽  
T Helper ◽  
Helper Cell Type

Myelin basic protein in CSF as indicator of disease activity in multiple sclerosis

1998 ◽  
Vol 4 (3) ◽  
pp. 124-126 ◽  
Author(s):  
K.J.B. Lamers ◽  
H.P.M. de Reus ◽  
P.J.H. Jongen
Keyword(s):  
Multiple Sclerosis ◽  
Disease Activity ◽  
Myelin Basic Protein ◽  
Basic Protein

The expression of integrins on activated T-cells in multiple sclerosis. Effect of intravenous methylprednisolone treatment

1998 ◽  
Vol 4 (3) ◽  
pp. 239-242 ◽  
Author(s):  
S Luján ◽  
J Masjuan ◽  
E Roldán ◽  
L M Villar ◽  
P González-Porqué ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cells ◽  
Total Population ◽  
Intravenous Methylprednisolone ◽  
Activated T Cells ◽  
Mean Intensity ◽  
T Cell Migration ◽  
Relapsing Remitting ◽  
Methylprednisolone Treatment ◽  
The Mean

We studied the effect of intravenous methylprednisolone (MP) on the expression of the integrins, LFA-1 and VLA-4, on activated blood T-lymphocytes in 17 patients with relapses of clinically definite relapsing-remitting MS. MP treatment did not induce changes in the expression of CD3, CD4, DR, LFA-1 or VLA-4 markers when measured in the total population of lymphocytes in MS patients in relation to treatment. Treatment influenced neither the LFA-1 nor VLA-4 positive cells within the CD3+ population. MP treatment clearly decreased the DR+ CD3+ cells (P50.01) and the percentage of DR+ CD3+ lymphocytes bearing VLA-4 (P50.01). However, this was not the case when we studied the percentage of lymphocytes which expressed LFA-1. Glucocorticoids did not influence the mean intensity of the expression of the two integrins quantified in either total or DR+ CD3+ lymphocytes. Although, further research seems warranted to investigate a possible effect of MP on lymphocyte integrin function, this work corroborates the idea that MP treatment may interfere with the mechanisms of T-cell migration into CNS, thus modulating the activity of multiple sclerosis.

Effect of monthly intravenous cyclophosphamide in rapidly deteriorating multiple sclerosis patients resistant to conventional therapy

2001 ◽  
Vol 7 (3) ◽  
pp. 185-188 ◽  
Author(s):  
Omar A Khan ◽  
Marina Zvartau-Hind ◽  
Christina Caon ◽  
Moeen U Din ◽  
Mickey Cochran ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Conventional Therapy ◽  
Clinical Deterioration ◽  
Intravenous Methylprednisolone ◽  
Intravenous Cyclophosphamide ◽  
Relapsing Remitting ◽  
Methylprednisolone Treatment ◽  
Multiple Sclerosis Patients ◽  
Relapsing Remitting Multiple Sclerosis ◽  
Clinical Worsening

Fourteen consecutive clinically definite relapsing-remitting multiple sclerosis (MS) patients were treated with monthly intravenous cyclophosphamide (CTX) for 6 months. All had experienced severe clinical deterioration during the 12 months prior to treatment with CTX despite treatment with conventional immunomodulating agents and intravenous methylprednisolone. Treatment with CTX led to improvement and neurologic stability within 6 months which was sustained for at least 18 months after the onset of treatment with CTX. Therapy with CTX was well tolerated. CTX may be of benefit in MS patients who experience rapid clinical worsening and are resistant to conventional therapy.

Myelin basic protein-like material in the urine of multiple sclerosis patients: relationships to clinical and neuroimaging changes

1998 ◽  
Vol 4 (3) ◽  
pp. 243-246 ◽  
Author(s):  
John N Whitaker
Keyword(s):  
Multiple Sclerosis ◽  
Myelin Basic Protein ◽  
Clinical Utility ◽  
Basic Protein ◽  
Progressive Multiple Sclerosis ◽  
Group Data ◽  
Relapsing Remitting ◽  
Cryptic Epitope ◽  
Multiple Sclerosis Patients

Urinary myelin basic protein-like material (MBPLM) represents material which is cross-reactive with a cryptic epitope in peptide 84-89 of human myelin basic protein. While normally present at moderate levels in the adult, these levels rise higher in patients who have secondary progressive multiple sclerosis (MS). The increase in urine MBPLM correlates with the burden of disease detected by T2-weighted cranial magnetic resonance imaging. There is no correlation between urinary MBPLM and acute disease activity in relapsing-remitting MS. The first major need for improving the clinical utility of measurements of MBPLM in urine in MS patients is to delineate its exact chemical features so that assays may be improved and a potential biological role of the MBPLM better understood. The second major task is to apply the group data accumulated and apply them to individual patients. This could prove to be means to individually direct treatment and determine its effectiveness.

scholarly journals Visualization of Myelin Basic Protein (Mbp) T Cell Epitopes in Multiple Sclerosis Lesions Using a Monoclonal Antibody Specific for the Human Histocompatibility Leukocyte Antigen (Hla)-Dr2–Mbp 85–99 Complex

2000 ◽  
Vol 191 (8) ◽  
pp. 1395-1412 ◽  
Author(s):  
Michelle Krogsgaard ◽  
Kai W. Wucherpfennig ◽  
Barbara Canella ◽  
Bjarke E. Hansen ◽  
Arne Svejgaard ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cell ◽  
Myelin Basic Protein ◽  
Basic Protein ◽  
Interleukin 2 ◽  
Disease Process ◽  
T Cell Epitopes ◽  
Structural Requirement ◽  
Leukocyte Antigen ◽  
Peptide Complexes

Susceptibility to multiple sclerosis (MS) is associated with the human histocompatibility leukocyte antigen (HLA)-DR2 haplotype, suggesting that major histocompatibility complex class II–restricted presentation of central nervous system–derived antigens is important in the disease process. Antibodies specific for defined HLA-DR2–peptide complexes may therefore be valuable tools for studying antigen presentation in MS. We have used phage display technology to select HLA-DR2–peptide-specific antibodies from HLA-DR2–transgenic mice immunized with HLA-DR2 molecules complexed with an immunodominant myelin basic protein (MBP) peptide (residues 85–99). Detailed characterization of one clone (MK16) demonstrated that both DR2 and the MBP peptide were required for recognition. Furthermore, MK16 labeled intra- and extracellular HLA-DR2–MBP peptide complexes when antigen-presenting cells (APCs) were pulsed with recombinant MBP. In addition, MK16 inhibited interleukin 2 secretion by two transfectants that expressed human MBP–specific T cell receptors. Analysis of the structural requirement for MK16 binding demonstrated that the two major HLA-DR2 anchor residues of MBP 85–99 and the COOH-terminal part of the peptide, in particular residues Val-96, Pro-98, and Arg-99, were important for binding. Based on these results, the antibody was used to determine if the HLA-DR2–MBP peptide complex is presented in MS lesions. The antibody stained APCs in MS lesions, in particular microglia/macrophages but also in some cases hypertrophic astrocytes. Staining of APCs was only observed in MS cases with the HLA-DR2 haplotype but not in cases that carried other haplotypes. These results demonstrate that HLA-DR2 molecules in MS lesions present a myelin-derived self-peptide and suggest that microglia/macrophages rather than astrocytes are the predominant APCs in these lesions.

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