Chronic Myeloid Leukemia: CD86 Expression Predicts Relapse
PD1- or CTLA-4-blocking antibodies may help to reduce the likelihood of relapse by increasing T cell proliferation.
CD86 expression on plasmacytoid dendritic cells (pDC) may predict chronic myeloid leukemia (CML) recurrence among patients who discontinue tyrosine kinase inhibitor (TKI) treatment, according to a study published in Leukemia.1
Some patients who discontinue TKI treatment eventually relapse, making timing of discontinuation controversial. Research suggests that treatment-free remission is achieved via immune-mediated disease repression; CD86 expression on pDC may reduce T cell activation, limiting this repression. For this study, researchers evaluated whether CD86 expression affects likelihood of CML relapse.
Patients were enrolled from the CML-V study (ClinicalTrials.gov Identifier: NCT00002869) and the EURO-SKI trial (ClinicalTrials.gov Identifier: NCT01596114). CD86 expression on pDC was analyzed in 144 patients from CML-V post-TKI discontinuation and in 122 patients from EURO-SKI prospectively.
Among patients from EURO-SKI, 1-year relapse-free survival (RFS) was 30.1% when CD86+ pDC was high (more than 95 per 105 lymphocytes); 1-year RFS was 70% when CD86+ pDC was fewer than 95 per 105 lymphocytes.
High CD86+ pDC frequencies were found in both patient groups when compared to normal donors. High CD86+ pDC predicted relapse both at baseline and post-TKI discontinuation.
Among patients from the CML-V study in molecular remission, those treated with nilotinib had a higher CD86+ pDC frequency.
The authors concluded that the frequency of CD86 expression on pDC predicts CML relapse. PD1- or CTLA-4-blocking antibodies may help to reduce the likelihood of relapse by increasing T cell proliferation; a study is being designed to evaluate this.
- Schutz C, Inselmann S, Sausslele S, et al. Expression of the CTLA-4 ligand CD86 on plasmacytoid dendritic cells (pDC) predicts risk of disease recurrence after treatment discontinuation in CML. Leukemia. 2017 Jan 11. doi: 10.1038/leu.2017.9 [Epub ahead of print]