Possible new targets for the treatment of myelodysplasia syndromes have been identified by US researchers.
Dr Daniel Starczynowski and colleagues at Cincinnati Children's Hospital Medical Center, USA, investigated the role of toll-like receptor activation in myelodysplastic syndromes, which frequently develop into cancer.
In mouse haematopoietic stem/progenitor cells, they found an overexpression of an effector cytokine called TRAF6. Effector cytokines worked to direct the adaptive immune response. Overexpression of TRAF6 in these cells leads to impaired blood cell development and bone marrow failure, likely triggering myelodysplastic syndromes in some cases, they report.
In Nature Immunology recently, the team states that TRAF6 normally functions as an immune sensor of pathogens.
Further tests of human leukaemia cells highlighted a substance in TRAF6 called hnRNPA1, involved in RNA binding, which could be potential treatment targets for cases of myelodysplastic syndromes triggered by overexpression of TRAF6.
Dr Starczynowski says: "Based on our paper, a number of therapeutic approaches can be tested and directed against TRAF6 and other related proteins responsible for myelodysplastic syndromes."
He adds that, in response to various pathogens, TRAF6 also regulates an important step in the translation of genetic code, called RNA isoform expression. This process is important to the function of haematopoietic cells and reveals another dimension to how cells respond to infection, say the team.
They now plan to test the therapeutic potential of the new targets identified in this study.
Source: Fang, J. et al. Ubiquitination of hnRNPA1 by TRAF6 links chronic innate immune signaling with myelodysplasia. Nature Immunology 26 December 2016; doi: 10.1038/ni.3654
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