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. Author manuscript; available in PMC: 2014 May 6.
Published in final edited form as: Leukemia. 2013 Jun 14;27(9):1832–1840. doi: 10.1038/leu.2013.180

Figure 6. Clinical analysis and proposed model of TLR2 mediated innate immunity signaling in MDS.

Figure 6

(a) Higher TLR2 expression level in low-risk patients compared to others. (b) Distinct TLR6 expression levels in high-risk, intermediate-1 and 2, and low-risk patients. (c–d) Correlation of TLR2 and 6 with overall survival of patients. (e) Patients with TLR2-F217S are with higher frequency of 7-/7q-. (f) Proposed model of a potential TLR2-JMJD3-IL8 signaling axis is abnormally activated in BM CD34+ cells of MDS. This abnormal activation includes overexpression of TLR1, 2 and 6, as well as genetic alteration (F217S) of TLR2. This signal axis leads to consequent activation of JMJD3 and IL-8. JMJD3 can also positively regulate both genes of IL8 and its receptor in MDS BM CD34+ cells. Impact of this innate immunity signaling contributes to the pathogenesis of MDS.