Immunoregulation at Mucosal Surfaces

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Background

The epithelia lining the surfaces of the body are sites of interactions between microbes, tissue cells and the immune system. The epithelium provides the first line of defense and serves as afferent sensor of danger present within the luminal microenvironment by secreting chemokines and cytokines that alert and direct innate and adaptive immune responses. The innate immune cells a second line of defense. Intestinal dendritic cells also have an immunosensory role being activated by specific microbial-associated molecular patterns, sampling antigens and traveling to the mesenteric lymph node. Also, ILCs are important effector cells of the innate immune system that are predominantly found at mucosal sites. The third sensory line is represented by sensory neurons detecting harmful environmental challenges. The term “gut-brain-axis” illustrates the bidirectional communication between the central nervous system (CNS) and the intestine. The enteric nervous system (ENS) transmits afferent/sensory information to the CNS, and receives efferent signals from the CNS. The nervous system is a regulator of the immune function and cells of both, the innate and adaptive immune system could be targeted by a wide range of neurotransmitters and neuropeptides. In this way the ENS may therefore be considered as an unprecedented player in immune homeostasis at mucosas.

The microbiota at mucosal surfaces can have both beneficial and deleterious effects. Mucosal associated lymphoid tissue discriminates between the commensal microbiota and potential pathogenic microorganisms, inducing specific immunity towards pathogenic agents or displaying tolerance towards commensal microbes. Many of the metabolites derived from commensals can impact host health by directly regulating the immune system. Dysbiosis is involved in autoimmune development in both mice and humans.

Growing interest has emerged in understanding the activation, differentiation and plasticity of different ILCs and T helper cell subsets. Recent studies have indicated that the ENS plays a role in the activation of ILCs. Neuronal regulation of ILCs via multiple neuropeptides and neurotransmitters and the corresponding receptors expressed by ILCs, DCs and other immune cells emerged as an important signaling hub in tissues for integration of body homeostasis and immunity at barrier surfaces.

Furthermore, both lymphoid and myeloid cell populations located at mucosal surfaces are highly reactive to cues from the environment, for example from the diet. Tissue location of certain immune cell types can depend on the energy content of food, and dietary metabolites modulate differentiation and function of immune cells.

The challenge in the upcoming years will be to uncover the basis of these tissue-resident circuits, which regulate inflammation and tissue homeostasis in health and disease. This Research Topic aims to provide a comprehensive overview of our current understanding of these elements. We therefore welcome the submission of Original Research, Review and Mini-Review articles that cover, but are not limited to, the following topics:

1. Control of mucosal immunity by innate and adaptive immune cells
2. Control of immune responses at mucosal surfaces by microbiota, metabolites and nutrients
3. Control of systemic immune responses from mucosal surfaces
4. Neuroimmune modulation at mucosal barriers
5. Role of innate and adaptive immune cells in response to microbes at mucosal surfaces.
6. Regulation of host immune responses by probiotics.
7. Therapeutic potential of immunoregulation at mucosal surfaces in inflammatory and autoimmune diseases.

Keywords: microbiota, T cell subsets, innate lymphoid cells, autoimmunity, tolerance, probiotics, neuroimmune.

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.

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