Innate lymphoid cells – New players in tissue injury and repair?

This presentation was given by Jan-Eric Turner from III. Medical Clinic of University Medical Center Hamburg in Germany. It was presented at the ISN’s Forefronts Symposium 2015 taking place in Shenzhen, China, on October 22-25, 2015 for which the theme was ‘Immunomodulation of Cardio-Renal Function’ during Session 2: Innate and Adaptive Immunity and Renal Pathology.


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Presentation Abstract:

In the last few years a population of lymphocytes that belongs to the innate arm of the immune system has been identified and studied extensively. Because of their antigen-independent activation and lymphoid morphology these cells have been termed “innate lymphoid cells” (ILC). According to the most recent nomenclature, conventional NK cells, that share characteristics of innate lymphoid cells, are considered to be part of the ILC family and have been referred to as “killer” ILC. The family of “non-killer” ILCs (also “helper-like” ILC) can be further divided into three groups that differ in their cytokine production, transcription factor usage, tissue localization and functional characteristic. The transcriptional programmes and effector cytokines of ILC are similar to that of the T helper cell subsets, suggesting that ILC represent an innate group of specialised cytokine producers that exist in parallel to the established system of T helper cells. The interaction of ILC with cells of the adaptive immune system and their contribution to the overall amount of cytokines produced in different settings and phases of the immune response are in the focus of ongoing studies.

Early after their description as an independent population of lymphocytes, important functions of ILC have mainly been identified in barrier organs, such as the gut, lung and skin. Since then, extensive research in the field has demonstrated that ILC are an essential part of the immune system in a variety of different organs during homeostasis and infection. Functions of ILC include the maintenance of gut barrier function, the immunity against various pathogens, autoimmune inflammation in the skin and intestine, as well as metabolic control in adipose tissues. In recent studies by us and others, it has been shown that IL-5- and IL-13-producing ILC are crucial for the regulation of eosinophil abundance and the differentiation of alternatively activated macrophages. Thereby, and by producing mediators that directly enhance epithelial growth, these ILC can contribute to tissue remodelling and repair after acute tissue injury. On the other hand, by employing similar cytokine pathways they can have deleterious effects for progression of organ fibrosis.

First evidence indicates that expansion of ILC by systemic cytokine treatment can enhance tissue repair in mouse models of kidney injury. Furthermore, we were able to identify an ILC population in the human kidney, suggesting that these cells might also contribute to human kidney disease. The role of ILC subtypes in the kidney as a source of T helper-cell-associated cytokines and their function in renal inflammation and fibrosis await further study. The long-term aim will be to evaluate renal ILC as a potential therapeutic target for modulation of the immune response in inflammatory kidney diseases.

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