Expression of both MCL1 and BCL2A1 has, in several hematological malignancies, been associated with chemoresistance or poor prognosis [34, 35]; thus, new drugs targeting these proteins must be developed.
This resistance is associated with a robust coexpression of MCL1 and BCL2A1 and is dependent on IL-17A that induces BCL2A1 in MCL1+ DC .
IL-17A- and IFN-[gamma]-treated DCs also underwent apoptosis upon addition of antibodies neutralizing IL-17A, which selectively reduced BCL2A1 expression.
Two genes were common in both lists: CCL4 and BCL2A1. This is a strong argument to further evaluate the role of BCL2A1 in RA and, in particular, a potentially overlooked role of long-term surviving IL-17A-stimulated [MCL1.sup.+] [BCL2A1.sup.+]-activated DCs.
Targeting MCL1 and BCL2A1 in Langerhans Cell Histiocytosis
Considering the presence also of IL-17A in LCH and the therapeutic efficacy of vinblastine, targeting MCL1, it would be interesting to study the role of MCL1 and BCL2A1 in LCH and to correlate their expression to disease progress and drug resistance.