TYK2-deficient PBMC showed divergent responses to IL-10 and
IL-6
IL-10 signals via IL-10R1 and IL-10R2, which associate with JAK1 and
TYK2, respectively [17]. IL-6 can also induce
phosphorylation of TYK2. Similarly, we assessed the responses of PBMC
from TYK2-deficient patients to IL-10 and IL-6. PBMC from P1 showed
intact response to IL-6 but abolished response to IL-10 as evidenced by
the phosphorylation of STAT3 (Fig. 3A).
PBMC from P2 showed significantly
impaired responses to both IL-6 and IL-10 as evidenced by the
phosphorylation of STAT3 (Fig. 3B), in contrary to P3, whose responses
to IL-10 and IL-6 seemed normal as evidenced by the phosphorylation of
STAT3 (Fig. 3C) and the transcription of SOCS3 (Fig. 3D), a STAT3 target
gene. These data again showed the role of TYK2 in IL-10 and IL-6
signaling was complicated as previously reported.