By G. Da Silva Xavier
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Extra resources for Advances in Protein Kinases
2011). Remarkably, these effects occur regardless of whether the JAK2V617F allele is present. Therefore, determining exactly how this class of drugs can exert its effects is necessary if clinical efficacy is to be improved. It has been suggested that the lack of selectivity of ruxolitinib may be responsible for its limited efficacy in PMF, but comparable studies with more selective inhibitors such as LY3009104 (Lilly, currently in phase II trials for RA), which is approximately 40-fold more selective for JAK2 versus JAK1, will be required to address this issue.
2008). IL-6 has also been found to suppress generation of Treg cells, which restrain effector T cell responses (Hirano, 2010). The balance between these two subsets is critical for maintaining homeostasis, and so the ability of IL-6 to drive the balance in favour of Th17 cell dominance is likely to be a be a major cause of pathology in RA and other disorders. , 2006). These observations demonstrate that IL-6-regulated immune and non-immune cell interactions are critical in the development of RA, and suggest that such interactions may play a similar etiological role in other autoimmune diseases in which IL-6 plays an integral role such as psoriasis, uveitis and inflammatory bowel disease.
Scheller, J. (2011) The soluble Interleukin 6 receptor: generation and role in inflammation and cancer, Eur J Cell Biol. 90: 484-494. A. H. (1988) The leukocyte common antigen (CD45): a putative receptor-linked protein tyrosine phosphatase, Proc Natl Acad Sci U S A. 85: 7182-7186. S. & Wang, D. (2003) Identification of Shp-2 as a Stat5A phosphatase, J Biol Chem. 278: 16520-16527. P. L. (2002), Attenuation of leptin action and regulation of obesity by protein tyrosine phosphatase 1B, Dev Cell.