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T. Mährle et al.
drug.36 It is also in line with the observed upregulation of PAX5, a gene involved in V(H)DJ(H) recombination of pro- B cells, in lenalidomide responders described in a BM RNA sequencing study of patients with non-del(5q) MDS, sug- gesting that this drug non-specifically expands the B line- age pool by this mechanism.19
The BM T-cell space in patients with del(5q) MDS was significantly more restricted than that of PB indicating T- cell-mediated immunity in the BM niche where T cells are in direct contact with the del(5q) MDS clone. The BM T- cell repertoire was much more conserved over time than the B-cell repertoire with a higher clonal overlap between
A
B
Figure 2. Clonal overlaps in T- and B-cell environments of patients with del(5q) myelodysplastic syndromes. Individual (A) IGH or (B) TRB repertoires in the peripheral blood and bone marrow of patients with del(5q) myelodysplastic syndromes before and after lenalidomide treatment were matched to each other. The absolute numbers of shared CDR3 sequences between the samples are shown. Pat.: patient; PB: peripheral blood; BM: bone marrow; MDS; myelodysplastic syndrome; baseline: prior to lenalidomide treatment; post lena: after lenalidomide treatment, NA: not analyzed.
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