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. 2022 May 10;13:902853. doi: 10.3389/fimmu.2022.902853

Figure 1.

Figure 1

Mechanisms of viral inhibition by IL-27. IFN-dependent: (A) IL-27 promotes the production of type I and III IFNs which leads to transcription of ISGs (20, 23, 29). (B) IL-27 induced by type I IFNs leads to expression of TRIM25 (21). (C) IL-27 complexes with sIL-6R and increases production of type I and III IFNs, leading to transcription of several ISGs (31, 33, 34). (D) IL-27 promotes the production of type II IFN by T cells and NK cells (28, 35, 51–54). (E) IL-27 promotes pDC differentiation, leading to increased IFN production (39). IFN-independent: (F) IL-27 directly promotes the transcription of several ISGs (19, 25, 27, 32, 38, 55). (G) IL-27 induces the expression of miRNAs that potentially target several viruses (56, 57). (H) IL-27 enhances the expression and signaling capacity of TLRs, which could influence recognition of PAMPs and DAMPs during viral infection (10–15). (I) IL-27 increased pro-inflammatory cytokine and chemokine production (40). (J) IL-27 promotes IL-10 production by T cells to mediate immunopathology during viral infection (18, 36, 37, 41, 58–61). (K) IL-27 enhances NK cell function by increasing granzyme B, RANTES, GM-CSF, and MIP-1α (28, 39).