Key signaling pathways related to IE-IRFs. IRFs primarily mediate the expression of ISGs from the ISRE in response to activation of IFNRs and PRRs. Dysregulation in these pathways leads to distinct clinical immunodeficiencies (IRF1, IRF3, IRF4, IRF7, IRF8, IRF9) or developmental syndromes (IRF6). (A) Upon binding the ISRE, IRF1 induces expression of a subset of ISGs. (B) IRF3 and IRF7 stimulate type I, II, and III interferon production. (C) IRF4 is crucial for lymphocyte development through interaction with the ISRE and AICE motifs. (D) IRF6 regulates genes required for epithelial differentiation and palate fusion. (E) IRF8 promotes lymphocyte development through interaction with the ISRE. (F) IRF9 complexes with STAT1 and STAT2 to form ISGF3, which drives ISG expression. AICE = AP-1-IRF composite element; EMT = epithelial–mesenchymal transition; and IFNRs, IFN receptors. Created in BioRender, https://BioRender.com/3h8qi1u.
Figure 2.

Key signaling pathways related to IE-IRFs. IRFs primarily mediate the expression of ISGs from the ISRE in response to activation of IFNRs and PRRs. Dysregulation in these pathways leads to distinct clinical immunodeficiencies (IRF1, IRF3, IRF4, IRF7, IRF8, IRF9) or developmental syndromes (IRF6). (A) Upon binding the ISRE, IRF1 induces expression of a subset of ISGs. (B) IRF3 and IRF7 stimulate type I, II, and III interferon production. (C) IRF4 is crucial for lymphocyte development through interaction with the ISRE and AICE motifs. (D) IRF6 regulates genes required for epithelial differentiation and palate fusion. (E) IRF8 promotes lymphocyte development through interaction with the ISRE. (F) IRF9 complexes with STAT1 and STAT2 to form ISGF3, which drives ISG expression. AICE = AP-1-IRF composite element; EMT = epithelial–mesenchymal transition; and IFNRs, IFN receptors. Created in BioRender, https://BioRender.com/3h8qi1u.

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