By Augusto Vaglio
This booklet offers specific details at the nosology, pathology, pathogenesis, medical presentation, analysis and therapy of fibro-inflammatory problems, infrequent ailments that regularly show systemic organ involvement. one of the stipulations thought of are IgG4-related disorder, sclerosing cholangitis, Hashimoto’s and Riedel’s thyroiditis, retroperitoneal fibrosis/chronic periaortitis, mediastinal fibrosis, Erdheim-Chester disorder, gadolinium-induced fibrosis, and sclerosing mesenteritis. This crew of entities remains to be poorly outlined and is characterised by way of the typical denominator of power inflammatory infiltrate admixed with ample fibrosis. IgG4-related sickness is the prototypical instance. Systemic Fibroinflammatory Disorders is the 1st e-book to attract jointly details on those stipulations. As those illnesses frequently require an interdisciplinary procedure, the e-book is addressed to experts of other disciplines, specifically internists, rheumatologists, nephrologists, scientific immunologists, and hematologists.
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Extra info for Systemic Fibroinflammatory Disorders
In red, anti-fibrotic cytokines. In purple, cytokines known to enhance the pro- inflammatory activity of fibroblasts but with no direct pro-fibrotic activity. + denotes activation. − denotes inhibition. CTGF connective tissue growth factor, ECM extracellular matrix, IL interleukin, PAI-1 plasminogen activator inhibitor 1, PDGF platelet-derived growth factor, TGF-β transforming growth factor-β, TNF tumor necrosis factor nuclear translocation. This signaling cascade is negatively regulated by SMAD7 .
Thus, inflammation and fibrosis are tightly associated when the integrity of a tissue is at stake and tightly associated when the fibrotic process goes beyond repair and becomes itself the source of pathology. In practical terms there is no fibrosis in the absence of inflammation. A variety of cell types and soluble mediators contribute to the initiation, full progression, and then the resolution of inflammation. A given cell type or a given soluble factor may play different roles (sometime opposite roles) in the inflammatory process according to the timing and environment in which it enters in action.
Interleukin-4 (IL-4) and IL-13 Classical Th2 cell products, such as IL-4 and particularly IL-13, have been shown to have direct and indirect roles in fibrosis development. IL-4 and IL-13 enhance type I collagen production in dermal fibroblasts [78, 79]. IL-13 in vivo acts by inducing TGF-β production by macrophages and directly stimulating myofibroblast and fibroblast synthetic activities. IL-13 function is regulated by the relative expression of the two IL-13 receptor subunits, IL-13Rα1 (signaling component) and IL-13Rα2 (decoy component).
Systemic Fibroinflammatory Disorders by Augusto Vaglio