CCR2/CCR6 deficient mice fail to recruit Ly6C+ monocytes and are thus protected from CCL4-induced hepatic fibrosis [251,252].
But DAT knock-down mice fail to mimic the observed sensorimotor deficits in PPI observed in humans (Ralph-Williams et al. 2003).
In further support of this, Lrp6+/− Lrp5−/− female mice fail to develop mammary ducts (Fig. 3E).
IL-6 and IL-12 deficient mice fail to respond to experimental autoimmune encephalomyelitis (EAE) [25], [26].
This contention is further supported by the finding that single S6K mutant mice fail to reveal a defect in T cell development [43], [44].
In this context, DCs from CCR7 deficient mice fail to form dermal "cords" at the dermal lymphatic vessels, and show impaired migration into LN.
Consistently, podocalyxin-deficient mice fail to form foot processes and slit diaphragms and die within 24 h after birth with anuric renal failure [39].
Notably, in agreement to our finding, macrophages from dectin-1 knockout mice fail to produce proinflammatory cytokines in response to Aspergillus infection [14].
Physiologically, adult α9−/− mice fail to show classic OC responses, characterized by an inability of OC system to modulate OHC activity [17].
In this context, it has been reported that DCs from CCR7−/− mice fail to migrate into the lymph nodes [3], [5].
Atoh1 is essential for hair cell differentiation [50] and Atoh1-null mice fail to differentiate hair cells and supporting cells [37].
