About this Research Topic
Peripheral nerves are the conduit for sensory information to the central nervous system. Peripheral sensory neurons are unique in spanning vast anatomical regions, linking the spinal cord to the extremities via sensory ganglia, and in their ability to regenerate after insult. They are supported in this role by numerous resident ‘glial’ cells, which in turn interact with peripheral immune cells to maintain homeostasis.
Upon disease or injury, the cellular environment of the peripheral nerve changes dramatically. Infiltrating immune cells are dynamic in both time and space, resulting in a complex interplay of reacting cells that co-determine the outcome of pathology and play a pivotal role in several peripheral neuropathies.
Immune contributions to both disease promoting and resolving processes may alter nerve structure, function (e.g. sensitization), and the capacity for regeneration. Much of the functional evidence for immune involvement in peripheral neuropathies centers on soluble factors, such as cytokines, chemokines and antibodies. However, far less is known regarding the contribution of individual cellular effector mechanisms to sensory nerve function, particularly among infiltrating leukocytes.
Attributing specific effector functions to individual immune or glial cells in neuropathy would help with the development of targeted immunotherapeutics, bypassing the side-effects of commonly used immunosuppressive drugs.
Cellular immunity enables selective targeting of specific cells and structures within the nerve and ganglia, acting via membrane-bound receptors and ligands. Molecular epitopes expressed in healthy and diseased nerves, regulate the cellular engagement of specific immune cell populations within anatomically distinct regions of the peripheral nerve. Knowledge of these cell-to-cell interactions is critical to understanding immune-related pathological processes, as well as reparative mechanisms, which may fail in chronic diseases of the nerve, including neuropathic pain.
The rapid development of high-dimensional, single-cell analytical techniques stands to further inform the molecular and functional identity of cellular immunity within the peripheral nervous system in health and disease.
In this Topic we are collating novel research outputs highlighting the molecular mechanisms underlying immune, and glial cell engagement with specific cellular targets within the peripheral nervous system microstructure focusing on the consequences for sensory nerve function in health and disease.
To this aim, we welcome articles addressing, but not limited to, the following:
- Cellular immunity, including lymphocytes, myeloid cells, dendritic cells, mast cells, neutrophils, and other granulocytes, as well as resident glial cells of the nerve and sensory ganglia.
- Evidence for direct cell engagement mechanisms (e.g. activation or inhibition) via receptor signalling in innate or adaptive immune pathways.
- Mechanisms of immune receptor engagement with membrane-bound ligands on nerve resident cells, or with other infiltrating immune cells, such as antigen presentation.
- Evidence for modulation of local cell functions by soluble ligands released by enzymatic cleavage.
- Studies on novel cellular effector mechanisms within the peripheral nervous system related to any aspect of nerve regeneration, cell death/axon degeneration, pain.
"Topic Editor, Dr. Sebastien Talbot received a research contract from Nocion Therapeutics and from Cygnal Therapeutics. Topic Editor, Dr. Thiago Mattar Cunha received a grant from GSK-UK. Dr. Franziska, Denk is on the Advisory Board of Cellectricon. The other Topic Editors declare no potential conflicts of interest related to this Research Topic."
Keywords: Adaptive/Innate immunity, Inflammation, Immunotherapy, Myelination, Neuropathic pain
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.