Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously reported that cell suspensions prepared by mechanical dispersion of thymic tissue from myasthenia gravis (MG) patients spontaneously synthesise anti-acetyl-choline receptor autoantibodies (anti-AChR) in culture in many cases. We now find a 2-200-fold greater anti-AChR production if the cell suspensions are prepared with the proteolytic enzymes collagenase and dispase (THYC + D). This difference has been seen in seven of the first 10 cases tested. Using these enzymes, we now also find comparable anti-AChR synthesis by MG lymph node cells, confirming the presumed extra-thymic production of much of this autoantibody. The increased anti-AChR synthesis by THYC + D is not simply a mitogenic effect of the enzymes, but apparently depends on several distinct factors: (1) plasma cells are often isolated much more efficiently--particularly by dispase--than by mechanical dispersion of these tissues (or of 'normal' tonsil), and the same may also be true of specific B cells. (2) The greatly increased numbers of fibroblasts, macrophages and other adherent cell types exert 'feeder' effects which enhance anti-AChR and total IgG production non-specifically. (3) Specific antigen presenting cells (APC) may also be recovered more efficiently and selectively stimulate anti-AChR production by B memory cells. These results imply that APC, plasma cells, and perhaps also B memory cells are recovered from germinal centres much more efficiently by enzymic than by conventional dispersion, a conclusion that may be relevant to workers studying antibody forming and memory B cells in other systems or species.
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PMID:Greatly increased autoantibody production in myasthenia gravis by thymocyte suspensions prepared with proteolytic enzymes. 631 38

Matrix metalloproteinases (MMPs) are zinc-dependent enzymes involved in remodeling extracellular matrix and cell-matrix interactions. A pathogenic role of MMPs in neurological disorders is likely. This paper focuses on serological clinical aspects only. In multiple sclerosis, higher serum MMP-3 is seen during relapses. Lower serum MMP-8 and -9 levels correlate with fewer contrast-enhanced T(2)-weighted MRI lesions, and serum MMP-9 can be used in monitoring treatment. In myasthenia gravis, serum MMP-2, -3, and -9 levels are elevated in both generalized and ocular diseases. A proportion of the patients have markedly increased serum MMP-3. In acute stroke, higher serum MMP-9 correlates with larger infarct volume, stroke severity, and worse functional outcome, and serum MMP-3 is significantly lower than in several other neurological disorders and healthy controls. In amyotrophic lateral sclerosis, serum MMP-2 correlates with disease progression, and both serum MMP-1 and -2 are elevated. In Alzheimer's disease, serum MMP-3, -9, and -10 are elevated. In migraine, serum MMP-2 is elevated, and also MMP-9 in those patients with migraine without aura. MMP-9 is implicated in the pathogenesis of experimental epilepsy. A pathogenic role of MMPs in these conditions could be related to their ability to degrade extracellular matrix. MMPs may also facilitate autoimmunity.
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PMID:Serum levels of matrix metalloproteinases: implications in clinical neurology. 2226 94