In MyD88-independent pathway TRIF and TRAM adaptor proteins are involved in the activation of
TRAF3 and, downstream, in the induction of TBK1 and IKK[epsilon], needed for the activation of the transcription factor IRF3.
Expanding TRAF function:
TRAF3 as a tri-faced immune regulator.
In line with previous findings discussed above showing that NOD1/RIP2-mediated
TRAF3 activation triggers type I IFN responses rather than NF-[kappa]B-related responses, (10) Cdx2 expression induced by exposure to H.
In the TLR pathway, there were 8 key genes with a significant difference in expression (P < 0.05): RAC1,
TRAF3, MAPK3, IFNAR1, TICAM1, IL6, MAPK11, and IFNA1 (Table 5).
The enzyme, called
TRAF3, lives on to control a molecular network that is implicated in a variety of immune system-related diseases if left to its own devices.
On the other hand, the transcription factor IRF-7 (Interferon regulatory factor 7) can bind to the MyD88/IRAK1/IRAK4 complex, and its activation is dependent upon TLR7/TLR8 and TLR9, requiring the
TRAF3 (TNF receptor-associated factor 3) protein which joins IRAKI and IKKa kinases to produce interferon alpha (IFN-[alpha]) (7).
Characterization of LMP-1's association with TRAF1, TRAF2, and
TRAF3. J Virol 1997;71:4649-56.
IRF3 can be phosphorylated and nuclear translocated by IKK, TBK1, and IKKi (IKK[epsilon]) that can be activated by TRIF requiring
TRAF3 (Figure 1) [32, 33].
Brink, "TRAF2 and
TRAF3 signal adapters act cooperatively to control the maturation and survival signals delivered to B cells by the BAFF receptor," Immunity, vol.