First reported in 1999, IL-19 remains a mystery in many ways. Despite appearing in many genome scans and candidate gene studies, and having been searched for specifically as part of the IL-10 family, its function is still to be defined. Nonetheless, a pattern of Th2 promotion is coalescing from this nebulous body of work, supported by increasing evidence for a role in asthma. Similarly, a clear but less intuitive role as a subtle immunomodulator is emerging in psoriasis and chronic inflammatory disorders in general. Indeed, several human diseases and their animal models have highlighted a role for IL-19. Key questions remain, relating to the nature of its receptor, its function (if any) on leukocytes and how its effects are distinguished by the cell from those of IL-20 and IL-24. In this review, I shall attempt to bring together a summary of the known work - disparate as it may be - as well as presenting a picture of these two important clinical disorders and the potential involvement of this somewhat enigmatic cytokine.
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Interleukin-19 (IL-19) acts as a negative-feedback regulator to limit proinflammatory response of macrophages and microglia in autocrine/paracrine manners in various inflammatory diseases. Multiple sclerosis (MS) is a major neuroinflammatory disease in the central nervous system (CNS), but it remains uncertain how IL-19 contributes to MS pathogenesis. Here, we demonstrate that IL-19 deficiency aggravates experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, by promoting IL-17-producing helper T cell (Th17 cell) infiltration into the CNS.
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Cardiovascular disease remains a major medical and socioeconomic burden in developed and developing countries and will increase with an aging and increasingly sedentary society. Many vascular diseases and atherosclerotic vascular disease, in particular, are essentially inflammatory disorders, involving multiple cell types. Communication between these cells is initiated and sustained by a complex network of cytokines and their receptors.
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Department of Physiology, Independence Blue Cross Cardiovascular Research Center, Temple University School of Medicine, Philadelphia, PA 19140, USA. Electronic address:
Hypoxia in ischemic limbs typically initiates angiogenic and inflammatory factors to promote angiogenesis in attempt to restore perfusion. There is a gap in our knowledge concerning the role of anti-inflammatory interleukins in angiogenesis, macrophage polarization, and endothelial cell activation. Interleukin-19 is a unique anti-inflammatory Th2 cytokine that promotes angiogenic effects in cultured endothelial cells (EC); the purpose of this study was to characterize a role for IL-19 in restoration of blood flow in hind-limb ischemia, and define potential mechanisms.
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