Nociceptor neurons promote IgE class switch in B cells

Nociceptors, the high-threshold primary sensory neurons that trigger pain, interact with immune cells in the periphery to modulate innate immune responses. Whether they also participate in adaptive and humoral immunity is, however, not known. In this study, we probed if nociceptors have a role in distinct airway and skin models of allergic inflammation. In both models, the genetic ablation and pharmacological silencing of nociceptors substantially reduced inflammatory cell infiltration to the affected tissue. Moreover, we also found a profound and specific deficit in IgE production in these models of allergic inflammation. Mechanistically, we discovered that the nociceptor-released neuropeptide substance P helped trigger the formation of antibody secreting cells and their release of IgE. Our findings suggest that nociceptors, in addition to their contributions to innate immunity, play a key role in modulating the adaptive immune response, particularly B cell antibody class switching to IgE.

Automated summary

Nociceptors, high-threshold primary sensory neurons triggering pain, were found to play a key role in modulating adaptive immune responses in allergic inflammation models, particularly in B cell antibody class switching to IgE. Their interaction with immune cells not only affects innate immunity, but also influences IgE production in allergic inflammation.