Immune Cells in Renal Fibrosis: a Role for Dendritic Cells?

This presentation was given by Richard Kitching from the Centre for Inflammatory Diseases and Departments of Nephrology and Paediatric Nephrology, Monash Health Melbourne, Australia. 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 9: Immunity, Fibrosis and Kidney Disease.

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Presentation Abstract: 

Dendritic cells are one of a number of links between innate and adaptive immunity. They present antigens to stimulate, perpetuate and in some instances regulate adaptive immune responses. However, they also have the capacity to act as innate pro- or anti-inflammatory cells. Systemically, dendritic cells are critical in establishing and perpetuating immune responses, both healthy and aberrant. However, in the kidney there is also network of mononuclear phagocytes in the tubulointerstitium, many of which behave as dendritic cells. There is evidence that in health these cells act as sentinels and in disease have the potential to play a variety of different roles. In addition to their various functional roles, dendritic cells are different in different parts of the kidney. Glomerular dendritic cells seem to be uncommon (at least in health or acute disease) and there is evidence for significant phenotypic differences between cortical and medullary renal dendritic cells.

Understandably, fibrosis is often viewed as a “final common pathway” to end stage kidney disease. However, the drivers of persistent and progressive renal disease are many and varied. Active inflammatory and metabolic drivers of disease accelerate fibrosis and drive progressive fibrotic disease, but when chronic injury is advanced, fibrosis tends still to progress even in the absence of the ongoing inciting stimulus. Thus the roles of renal dendritic cells are not simple, and need to be considered in the context of their involvement as antigen presenting or local innate cells, the nature of the pathogenic process, and the involvement of the glomerulus, the cortical tubulointerstitium and the medulla in disease. Current evidence suggests that in antigen-independent renal fibrosis, while macrophages can promote progression, interstitial dendritic cells’ roles are less clear.