Abstract
Virus-like particle (VLP)-based anti-infective prophylactic vaccination has been established in clinical use. Although validated in proof-of-concept clinical trials in humans, no VLP-based therapeutic vaccination against self-proteins to modulate chronic disease has yet been licensed. The present review summarises recent scientific advances, identifying interleukin-13 as an excellent candidate to validate the concept of anti-cytokine vaccination. Based on numerous clinical studies, long-term elimination of IL-13 is not expected to trigger target-related serious adverse effects and is likely to be safer than combined targeting of IL-4/IL-13. Furthermore, recently published results from large-scale trials confirm that elimination of IL-13 is highly effective in atopic dermatitis, an exceedingly common condition, as well as eosinophilic esophagitis. The distinctly different mode of action of a polyclonal vaccine response is discussed in detail, suggesting that anti-IL-13 vaccination has the potential of outperforming monoclonal antibody-based approaches. Finally, recent data have identified a subset of follicular T helper cells dependent on IL-13 which selectively trigger massive IgE accumulation in response to anaphylactoid allergens. Thus, prophylactic IL-13 vaccination may have broad application in a number of allergic conditions.
Highlights
In an age dominated by an avalanche of monoclonal antibodies (MAb) hitting the market for a dizzying variety of conditions, one may ask why replacing this obvious successful model with a vaccine strategy is sensible at all
It is intriguing that TfH1 cells, which would mediate class switching in response to a Virus-like particle (VLP)-type vaccine, would be instrumentalised in this way to suppress the activity of TfH13 cells
IL-13 represents an excellent proof-of-concept target to validate anti-cytokine vaccination as a therapeutic strategy in humans based on validated
Summary
In an age dominated by an avalanche of monoclonal antibodies (MAb) hitting the market for a dizzying variety of conditions, one may ask why replacing this obvious successful model with a vaccine strategy is sensible at all. The answer to this question is four-fold. It will be much more accessible to patients (economics) It will have much broader applications thanks to the qualitatively different nature of a polyclonal vs a monoclonal immune response (see below for details). This review does not intend to deliver a broader review of the signalling, structure, or immunobiology of IL-13 which have been reviewed excellently recently elsewhere [1,2,3]
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