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Chapter 4 - Immunological Properties of Botulinum Neurotoxins
- Edited by Daniel Truong, University of California, Riverside, Dirk Dressler, Hannover Medical School, Mark Hallett, National Institutes of Health (NIH), Christopher Zachary, University of California, Irvine, Mayank Pathak, Truong Neuroscience Institute
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- Book:
- Manual of Botulinum Toxin Therapy
- Published online:
- 02 November 2023
- Print publication:
- 23 November 2023, pp 18-22
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Summary
Botulinum neurotoxin is used to treat a large number of muscle hyperactivity disorders, including dystonia, spasticity, and tremor; autonomic disorders such as hyperhidrosis, hypersalivation and various bladder disorders; and pain conditions, especially chronic migraine. Aesthetic applications have also become a large indication. Commercially available preparations of Bont/A and BoNT/B are listed.
The active component in all products is BoNT, a di-chain protein of 150 000 daltons. BoNT/A inhibits release of acetylcholine by cleaving the SNARE protein SNAP-25 while BoNT/B cleaves VAMP II. Since BoNT is a foreign protein, the human immune system may respond to it with the production of specific anti-BoNT antibodies (BoNT-AB).
The probability of developing BoNT-AB increases with the amount of BoNT applied at each injection series. Other drug- and patient-related factors might contribute to the immune response. Unspecific activation of the immune system as a possible risk factor for BoNT-AB formation is currently been discussed in connection with COVID-19 vaccination programs. A pre-activation of lymphocytes may have triggered BoNT/A-AB formation. In this chapter, a method is presented for the quantification of BoNT-AB in sera, the immune cell reactions to antigens are described and drug related immune responses are discussed.
Chapter 4 - Immunological properties of botulinum neurotoxins
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- By Hans Bigalke, Institute of Toxicology, Hannover Medical School, Hannover, Germany, Dirk Dressler, Movement Disorder Section, Department of Neurology, Hannover Medical School, Hannover, Germany, Jürgen Frevert, Institute of Toxicology, Hannover Medical School, Hannover, Germany
- Edited by Daniel Truong, Dirk Dressler, Mark Hallett, Christopher Zachary
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- Book:
- Manual of Botulinum Toxin Therapy
- Published online:
- 05 February 2014
- Print publication:
- 23 January 2014, pp 16-21
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Summary
Introduction
Botulinum neurotoxins (BoNTs) are used to treat a large number of muscle hyperactivity disorders including dystonia, spasticity, tremor and autonomic disorders (e.g. hyperhidrosis and hypersalivation), as well as facial wrinkles. Commercially available products differ with respect to serotype, formulation and purity. Not all products are approved in all countries. Serotype A-containing products are Botox (onabotulinumtoxinA), Dysport (abobotulinumtoxinA) and Xeomin (incobotulinumtoxinA), whereas NeuroBloc/MyoBloc (rimabotulinumtoxinB) contains serotype B. The active ingredient in all products is BoNT, a two-chain protein with a molecular weight of 150 kDa. BoNT type A (BoNT-A) inhibits release of the neurotransmitter acetylcholine by cleaving synaptosomal associated protein-25, a SNARE protein, while BoNT type B (BoNT-B) cleaves synaptobrevin (vesicle-associated membrane protein-2).
Since BoNTs are foreign proteins, the human immune system may respond to them with the production of specific anti-BoNT antibodies. The probability of developing such antibodies increases with the BoNT doses applied (Göschel et al., 1997; Lange et al., 2009). Whether other drug-related factors might contribute to immune responses is discussed below. Patient-related factors may also be involved in triggering antibody formation to BoNT. Recently, a patient was reported who was treated with abobotulinumtoxinA for several years with good results until he developed anti-BoNT-induced therapy failure after he received BoNT following a wasp sting (Paus et al., 2006). Since components of wasp poison are effective immunostimulants, a preactivation of lymphocytes may have triggered antibody formation against BoNT-A. In the following, a method is presented for the quantification of anti-BoNT in sera; the immune cell reactions to antigens are described and drug-related immune responses are discussed.
4 - Immunological properties of botulinum toxins
- Edited by Daniel Truong, Dirk Dressler, Mark Hallett
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- Book:
- Manual of Botulinum Toxin Therapy
- Published online:
- 28 July 2009
- Print publication:
- 12 February 2009, pp 23-28
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Summary
Introduction
Botulinum toxins are used to treat a large number of muscle hyperactivity disorders, including dystonia, spasticity, and tremor, autonomic disorders, such as hyperhidrosis and hypersalivation, as well as facial wrinkles. Commercially available products differ with respect to serotype, formulation, and purity. Not all products are approved in all countries. Serotype A-containing products are Botox®, Dysport®, Chinese BoNT-A (CBTX-A) and Xeomin®, whereas NeuroBloc®/Myobloc® contains serotype B. The active ingredient in all products is botulinum neurotoxin (BoNT), a di-chain protein with a molecular weight of 150 kDa. Botulinum toxin type A (BoNT-A) inhibits release of acetylcholine by cleaving the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein SNAP 25 while BoNT type B (BoNT-B) cleaves vesicle-associated membrane protein (VAMP) II. Since BoNTs are foreign proteins, the human immune system may respond to them with the production of specific anti-BoNT antibodies (BoNT-AB). The probability of developing BoNT-AB increases with the BoNT doses applied (Göschel et al., 1997). Whether other drug-related factors might contribute to immune responses is discussed below. Patient-related factors may also be involved in triggering BoNT-AB formation. Recently, a patient was reported who was treated with Dysport for several years with good results until he developed BoNT-AB-induced therapy failure after he received BoNT following a wasp sting (Paus et al., 2006). Since components of wasp poison are effective immunostimulants, a preactivation of lymphocytes may have triggered BoNT-A-AB formation.