《Table 1Phenotypes of genetic deletion of transcription factors in mice.》

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《作为免疫疗法靶点的FOXP3及其辅因子》

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Li et al.[55]have found that FOXP3 binds directly to Tip60，HDAC7，and HDAC9 at the N-terminal region to form a chromatin-remodeling complex.Although the association of HDAC7 with FOXP3 and Tip60 seems to be important in order for FOXP3 to repress the targeted gene[56]，the precise mechanism is as yet unknown.Since HDAC7 has little enzymatic activity and needs to form a complex with other factors such as HDAC3 in order to function[40]，HDAC7 may be important in recruiting other FOXP3 cofactors.However，deletion of HDAC6[41，57]，HDAC9[42，57]，sirtuin-1（SIRT1）[44，57，58，59]，or HDAC11[43]increases the acetylation level and overall expression of FOXP3，in addition to enhancing Treg functions.