With the development of cancer treatments, it has become a popular research focus that mesenchymal stem (or stromal) cells (MSCs) have the functional mechanisms that influence cancer progression. One of the underestimated mechanisms is secretion of highly specialized double-membrane structures called exosomes. Mesenchymal stem cells generate several exosomes that may act as paracrine mediators by exchanging genetic information. MSC-derived exosomes are microvesicles ranging from approximately 60-200 nm in size and detected in various body fluids. It has been demonstrated that MSC-derived exosomes are involved in tumor growth, angiogenesis, metastasis, and invasion. Furthermore, emerging evidence suggests that as natural nanocarriers, MSC-exosomes are responsible for multidrug resistance mechanisms, reverse effect of radiation injury, and immune regulation, which can be used in clinical applications for cancer therapy. The present review aims to briefly describe the properties and biological functions of MSC-exosomes in cancer progression and its possible clinical applications in the future.

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Autoantibodies against the major acute-phase reactant C-reactive protein (CRP) are frequently found in patients with lupus nephritis. Further defining the autoimmune epitopes on CRP may not only improve patient stratification but also, hint at mechanisms of CRP action. Herein, we show that amino acids 35-47 constitute the major epitope recognized by anti-CRP autoantibodies in patients with lupus nephritis. Notably, the presence of autoantibodies against amino acids 35-47 associated with more severe renal damage and predicted worse outcome. This epitope is exposed on CRP only after irreversible structure changes, yielding a conformationally altered form termed modified or monomeric CRP (mCRP). ELISA and surface plasmon resonance assays showed that amino acids 35-47 mediate the interaction of mCRP with complement factor H, an inhibitor of alternative pathway activation, and this interaction greatly enhanced the cofactor activity of complement factor H. In contrast, autoantibodies against amino acids 35-47 inhibited these actions of mCRP. Our results thus provide evidence for the generation of mCRP in a human disease and suggest that mCRP actively controls the pathogenesis of lupus nephritis by regulating complement activation. Therefore, amino acids 35-47 constitute a functional autoimmune epitope on CRP that can be targeted therapeutically and diagnostically.