Editorial: Neuroinflammation and Neuroautoimmunity in Peripheral Neuropathies: Old Players, New Roles

In the last two decades, great emphasis has been placed on neuroimmune interaction in neuropathy and neuropathic pain onset (1). The importance of the immune system and its mediators in orchestrating, cooperating, and/or supporting mechanisms triggering or facilitating peripheral painful and non-painful neuropathy has also been recognized. Despite growing and continuous interest (2) in this topic, the links and communication among all the players (immune cells, peripheral and central glia, neurons) are complex and new elements are still required to decipher the underlying processes in different pathological conditions. Although peripheral neuropathies are of different aetiology (traumatic, metabolic, iatrogenic, autoimmune, genetic), they share similar peripheral and central neurodegenerative and neuroinflammatory processes. In particular, accumulating evidence highlights the critical role of crosstalk among neural, glial, and immune cells (3–5). Physiological and aberrant communication among different cell types takes place through the release of mediators having a pro- or anti-inflammatory power able to determine a cell conformational, morphological, and/or functional change (phenotypical switch); this, in turn, amplifies and supports the neuroinflammation or, on the contrary, switches off or reduces the neuropathy progression and symptoms such as neuropathic pain. In light of this inclusive approach, in which all neuroimmune players are in a reciprocal relationship, the papers included in this Topic Research provide a multifaceted view of the topic, coming from different models of disease. The aim is to suggest new potential therapeutic targets to improve the quality of life of patients with these pathologies.