In 2014 we witnessed a rapid growth of the research and studies at the interface and intersection of neurosciences and immunology. This vast interdisciplinary area, often referred to as neuroendocrine immunology or neuroimmunology, also includes stress-immune interactions that may have complex and multifaceted impact on health and disease. Last year also brought some interesting developments and new conceptual trends to the field, and some of these were outlined here, on the BrainImmune site. What we feel stimulating and important is now highlighted and summarized below.
The norepinephrine (noradrenaline)-driven cold stress response is most likely the underlying mechanism involved in this phenomenon. The authors suggested that “it is important to consider ambient temperature when cancers (and perhaps other disorders) are modeled in mice”.
The TRPV1 receptor (transient receptor potential vanilloid type 1 ion channel) is a classical nociceptor or pain receptor. Samuel Bertin and colleagues, however, identified a ‘non-canonical’ function of the TRPV1 receptor. This includes its expression, involvement in TCR signaling and pro-inflammatory activities of T cells, and cytokine productionsuch as IFN-γ, IL-17A and TNF.
This mechanism may help explain the stress-induced increase of blood leukocytes (e.g. neutrophils and monocytes) or their traffic to experimental atherosclerotic lesions, as demonstrated by these researchers.
This cytokine-induced neuropathy enhances the susceptibility of mesenchymal stem cells (MSC) in the haematopoietic niche to cell death and may represent a key mechanism in the development of myeloproliferative neoplasms (MPNs).
This model includes skin sensory neurons triggering IL-23 production by dendritic cells, acting on T cells to induce IL-17 and IL-22, which, in turn, recruit locally leukocytes to drive a psoriasiform skin inflammation.