Selected article for: "activation stimulus and acute disease"

Author: Kang, Soo Jung; Kim, Nam Su
Title: Association of Toll-like receptor 2-positive monocytes with coronary artery lesions and treatment nonresponse in Kawasaki disease
  • Document date: 2017_7_31
  • ID: tk1bxztw_50
    Snippet: The inclusion of a relatively small number of patients in these in vestigations presents a limitation of our study, which might affect the results of our statistical analyses and lead to difficulties in showing the correlation between FTLR2% or sIL10 and the previously determined risk factors of CAL development and IVIG resistance. Another limitation might be the relatively shortterm followup of our patients, as CALs can form after 1 month of ons.....
    Document: The inclusion of a relatively small number of patients in these in vestigations presents a limitation of our study, which might affect the results of our statistical analyses and lead to difficulties in showing the correlation between FTLR2% or sIL10 and the previously determined risk factors of CAL development and IVIG resistance. Another limitation might be the relatively shortterm followup of our patients, as CALs can form after 1 month of onset of the disease. Additionally, as this was a prospective study, the FTLR2% and sIL10 before the initial treatment could have affected the subsequent results of the echocardiograms taken 1 month later. Moreover, the regulation and interaction of TLRs and inflammatory cytokines occur in a complex manner 12) ; therefore, further studies are needed to elucidate how FTLR2% and sIL10 correlate. We did not separate monocytes from the whole blood in our study, therefore a small number of cells other than monocytes may have been analyzed. However, in accordance with the aim of this study, that is to establish FTLR2% as a potential marker of KD severity and prognosis, we thought that the use of whole blood samples served as an easier and more appropriate approach. Furthermore, the CAL (−) group showed increased FTLR2% after the initial treatment compared to the CAL (+) group. We pro pose that, with time, other endogenous TLR2 ligands might be responsible for the delayed stimulation of TLR2, in addition to the initial stimulus responsible for the early activation 12) . This finding may limit the use of FTLR2% as a prognostic parameter after the initial treatment. Our study focused on the acute changes in CALs in KD at disease onset, so further longterm followup studies will be needed to elucidate the longterm effects of TLR2 on coronary arteries in KD. Additional investigations of ligands capable of TLR2 activation in KD would be helpful.

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