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. Author manuscript; available in PMC: 2019 Mar 19.
Published in final edited form as: Cell Rep. 2018 Dec 11;25(11):2992–3005.e5. doi: 10.1016/j.celrep.2018.11.056

Figure 6. Model of LT-HSC aging and inflammatory myeloid-bias.

Figure 6.

Shifts in clonal heterogeneity during LT-HSC aging affects the inflammatory response of LT-HSCs. The LT-HSC compartment is comprised of unbiased and myeloid-biased LT-HSCs. With age, the clonal distribution of LT-HSCs shifts towards myeloid-biased variants which express high levels of CD61. During acute inflammatory challenges, aged myeloid-biased LT-HSCs preferentially expand, leading to increased myeloid output. Several cell-intrinsic factors, including the transcriptional regulators Klf5, Ikzf1 and Stat3 may play a role in establishing a myeloid-biased differentiation program during aging and inflammation. Extrinsic factors, including inflammatory cytokines and growth factors secreted from other cell types may also play a role.