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doi:10.1038/ng.2996

Introduction A widespread understanding in the pathophysiology of chronic inflammatory autoimmune diseases, such as RA, affirms that the diseased tissue has high prevalence of macrophages, inflammatory mediators and necrotic monocytes lacking clearance via lymphatic system, which can become an inflammatory trigger in itself contributing to adaptive immune response [1, 2]

A cleaved form of IGF-1, glycine-proline-glutamate (GPE), prevents the death of tyrosine hydroxylase (TH) immunopositive neurons, and restores TH immunoreactivity in the substantia nigra compacta (SNc) and the striatum of a 6-hydroxydopamine (6-OHDA)-induced PD model [100]

APC mutations in colorectal tumors with mismatch repair deficiency

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C., Fisher, A., Ren, H., Valdez, M., Kodavanti, P