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Abstract
Excessive immune responses are detrimental to the host and negative feedback regulation
is crucial for the maintenance of immune-system integrity. Recent studies have shown
that phosphoinositide 3-kinase (PI3K) is an endogenous suppressor of interleukin-12
(IL-12) production triggered by Toll-like receptor (TLR) signaling and limits excessive
Th1 polarization. Unlike IRAK-M (IL-1 receptor-associated kinase-M) and SOCS-1 (suppressor
of cytokine signaling-1) that are induced by TLR signaling and function during the
second or continuous exposure to stimulation, PI3K functions at the early phase of
TLR signaling and modulates the magnitude of the primary activation. Thus, PI3K, IRAK-M
and SOCS-1 have unique roles in the gate-keeping system, preventing excessive innate
immune responses.