Acid sphingomyelinase deficiency does not protect from graft-versus-host disease in transplant recipients with Niemann-Pick disease.
نویسندگان
چکیده
performance of the GM-CSF affinity column used to isolate antibodies. If used repeatedly, is it possible that a proportion of high affinity anti–GM-CSF AAs from PAP sera used as a positive control would be retained on the GM-CSF column and released slowly during subsequent purifications of HC IgG? If PAP anti–GMCSF IgG contamination did occur, not only would it account for the immunoblot data given in Figure 1a in their paper,1 where radiolabeled GM-CSF was shown to bind to the bound (IgG) fraction from both HC and PAP IgG, but also for the positive results in bioassays. Evidence of absolute clearance of GM-CSF–bound proteins before column reuse would have been useful in eliminating this possibility. Finally, the functional assays used for GM-CSF, including those used for measuring neutralizing effects, do not appear to have been adequately controlled for specificity. Assays used for measuring GM-CSF activity are not specific as they can respond to a range of cytokines and can be affected by inhibitory components in sera.13 Therefore, if specificity for neutralizing GM-CSF is to be claimed, then it is necessary to show that the affinity-purified antibodies do not neutralize other cytokines, such as interleukin-3, which can be tested using the TF1 cell-proliferation assay.13
منابع مشابه
[Niemann-Pick disease types A and B].
The molecular basis of Niemann-Pick disease, type A and B, has been confirmed by detection of mutations causing deficiency of the acid sphingomyelinase activity in the patients. It has been shown that mutations, which cause no activity of acid sphingomyelinase, are responsible for the type A and mutations which cause residual activities of the enzyme are responsible for the type B. Acid sphingo...
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عنوان ژورنال:
- Blood
دوره 115 2 شماره
صفحات -
تاریخ انتشار 2010