A Persistent Immune Response to an Acute Virus 英文参考文献.docVIP

Open access, freely available online Synopses of Research Articles Manipulating Microtubules in Systemic Sclerosis DOI: 10.1371/journal.pmed.0020403 Systemic sclerosis (scleroderma or SSc) is the name for a group of progressive diseases, all of which involve the abnormal growth of connective tissue. They are chronic degenerative disorders in which there is widespread vascular deterioration and tissue loss. The recognition of SSc dates back many years. Indeed, the characteristic stretched thickening of the skin was probably ?rst described by Hippocrates. A more de?nitive description of the condition was made by Carlo Curzio in 1753, who described a patient as having wood-like skin with “tight family of proteins (R-Smads), some of which act to stimulate further TGFβ signaling, and others of which act to inhibit it.The microtubules regulate the R-Smad access to and activation by TGFβ receptors. Dong and colleagues were able to show that in this model of SSc, paclitaxel markedly suppressed the activation of two of the Smads, Smad2 and Smad3, and, hence, collagen deposition in SSc grafts.They also showed that the SSc grafts had increased neovessel formation relative to normal grafts, regardless of paclitaxel treatment, thus indicating that paclitaxel did not have a negative effect on angiogenesis. In fact, they found that the neovascular cells were likely derived from the mouse hosts. DOI: 10.1371/journal.pmed.0020403.g001 eyelids, dif?culty in opening her mouth, coldness of her skin.” The etiology of SSc is still not Suppression of Smad2 phosphorylation by paclitaxel in in SSc skin graft completely understood, but appears to be autoimmune. Downstream of the immune activation, the molecules that have been implicated are the pro?brotic cytokines, such as transforming growth factor-beta (TGFβ), interleukin-4 (IL-4), platelet-derived growth factor (PDGF), and connective tissue growth factor, all of which can cause ?brosis. In addition to the pro?brotic e