Potential model of the interactions between miR-142 and key transcription factors implicated in the pathway. At steady-state (top panel), the interplay between PU.1, Irf8, and Irf4 orchestrates the differentiation of CD4 and CD8 DCs. Heterodimeric binding of PU.1 and Irf8 induces expression of the MHC class II transactivator CIITA, which may be repressed by transcription factors such as Blimp1 to allow efficient induction of DC antigen presentation required for T-cell priming. Modulation of the PU.1/Irf4 complex by miR-142 (bottom panel) disrupts the generation of CD4 DCs and favors the generation of CD8 DCs. Because Irf4 is important for induction of other transcription factors including Blimp1, failure of CIITA repression leads to elevated DC activation and maturation and impaired CD4+ T-cell priming ability. miR-142 may thus regulate the balance of different transcription factors to guide the outcome of an immune response.

Potential model of the interactions between miR-142 and key transcription factors implicated in the pathway. At steady-state (top panel), the interplay between PU.1, Irf8, and Irf4 orchestrates the differentiation of CD4 and CD8 DCs. Heterodimeric binding of PU.1 and Irf8 induces expression of the MHC class II transactivator CIITA, which may be repressed by transcription factors such as Blimp1 to allow efficient induction of DC antigen presentation required for T-cell priming. Modulation of the PU.1/Irf4 complex by miR-142 (bottom panel) disrupts the generation of CD4 DCs and favors the generation of CD8 DCs. Because Irf4 is important for induction of other transcription factors including Blimp1, failure of CIITA repression leads to elevated DC activation and maturation and impaired CD4+ T-cell priming ability. miR-142 may thus regulate the balance of different transcription factors to guide the outcome of an immune response.

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