Titlebook: Complement Therapeutics; John D. Lambris,V. Michael Holers,Daniel Ricklin Book 2013 Springer Science+Business Media New York 2013 infectio

現(xiàn)代

Franz-Jürgen Delvos,Walter Schempp the alterative pathway of complement system, which constitutes a significant part of innate immunity in humans. Histologically, the hallmark observation is the isolated glomerular deposition of C3 complement in the absence of immune complexes. It is considered one of the C3 glomerulopathies, and it

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Adornment

https://doi.org/10.1007/978-94-015-8169-1ion; this is an ideal model for parsing the role of airway vasculature in rejection. Prior to the development of airway fibrosis in rejecting tracheal allografts, C3 deposits on the vascular endothelium just as tissue hypoxia is first detected. With the eventual destruction of vessels, microvascular

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Mixed Convolutions and Zak Transforms,on with a recombinant protein that contains the C3d-binding region of complement receptor (CR) 2. Iron-oxide nanoparticles darken (negatively enhance) images obtained by T2-weighted MRI. We have demonstrated that the CR2-targeted nanoparticles bind within the kidneys of mice with lupus-like kidney d

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Progress and Trends in Complement Therapeutics,l disorders involving abnormal complement activity or regulation, which include both acute and chronic diseases and affect a wide range of organs, diverse yet specifically tailored therapeutic approaches may be needed to shift complement back into balance. This chapter highlights the key changes in

Consensus

Inhibition of the Serine Proteases of the Complement System,mall-molecule drugs can be very efficient serine protease inhibitors, but they usually lack sufficient specificity. A promising approach to yield more specific compounds is the alteration of natural protease inhibitors through engineering or directed evolution resulting in new variants with fine-tun

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The Role of MASP-1/3 in Complement Activation,le to convert the proenzyme of Df to an active form in vitro. In addition, MASP-1 was able to activate MASP-2 and MASP-3 as C1r activates C1s. Thus, MASP-1 and MASP-3 seem to be involved in activation of both the lectin and alternative pathways.