Supplementary Figures S1-S7 from Human TET2-Mutant Clonal Hematopoiesis Expansion Is Driven by Distinct Inflammatory Signaling Responses in Stem Cells Versus Myeloid Progeny

Figure S1. Long term culture competition assays of TET2Mut human HSPCs, related to Figure 1. Figure S2. Transcriptional responses of human HSPCs and its myeloid progeny upon LPS challenge, related to Figure 2. Figure S3. Absence of selective advantage of TET2Mut HSPCs in humanized NBSGW mice, related to Figure 3. Figure S4. In vivo models triggering emergency myelopoiesis are associated with TET2-CH expansion, related to Figure 3. Figure S5. In an in vivo model of systemic inflammation, human TET2Mut HSCs exhibit a dampened transcriptional response, originated from steady-state epigenetic repression of JUN and FOS related to Figure 4. Figure S6. TET2Mut human HSPCs produce a distinct progeny with myeloid cell subsets prompted to produce exacerbated inflammatory response, related to Figure 5. Figure S7. TET2Mut myeloid progeny acquired characteristics of inflamed tissue monocytes and distinct macrophage differentiation, related to Figure 5.