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Paraneoplastic disorders and neuroimmunology

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The extraordinary expansion in the field of neuroimmunology witnessed in the last decade is not just in the number of neurological disorders now considered to have an immune basis, nor the depth of understanding of disorders long known to be ‘neuroimmune’. Nor is it in the number of antibodies discovered and now testable, nor in the range of new immune suppressant or modifying treatments now emerging or already available. It is of course all of these things, but it is also more than the sum of these parts. What we are currently privileged to witness is the coming together of immunological understanding, the neurobiology of disease, and rational immune therapy, or at least the beginning of this process. To take one isolated example, neurogenetics and neurophysiology taught us about the clinical consequences of channel disruption; laboratory-based neuroimmunology showed antibodies to be capable of producing comparable acquired disease; and it seems likely that specific anti-B-cell humanized monoclonal antibodies offer the therapeutic potential to remove these channel-disrupting antibodies. Neither of these steps could be described in the last edition, and one can imagine similar dramatic changes will emerge before the next.
Oxford University Press
Title: Paraneoplastic disorders and neuroimmunology
Description:
The extraordinary expansion in the field of neuroimmunology witnessed in the last decade is not just in the number of neurological disorders now considered to have an immune basis, nor the depth of understanding of disorders long known to be ‘neuroimmune’.
Nor is it in the number of antibodies discovered and now testable, nor in the range of new immune suppressant or modifying treatments now emerging or already available.
It is of course all of these things, but it is also more than the sum of these parts.
What we are currently privileged to witness is the coming together of immunological understanding, the neurobiology of disease, and rational immune therapy, or at least the beginning of this process.
To take one isolated example, neurogenetics and neurophysiology taught us about the clinical consequences of channel disruption; laboratory-based neuroimmunology showed antibodies to be capable of producing comparable acquired disease; and it seems likely that specific anti-B-cell humanized monoclonal antibodies offer the therapeutic potential to remove these channel-disrupting antibodies.
Neither of these steps could be described in the last edition, and one can imagine similar dramatic changes will emerge before the next.

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