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SHIP-1 regulates PI3 kinase signaling by dephosphorylating intracellular PIP3.
The SHIP-1−/− mice were generated as previously described [10].
We asked if SHIP-1−/− mice had altered mucus response.
Again, T cells from SHIP-1−/− mice did not respond well to either WT APC or SHIP-1−/− APC.
Furthermore, isolated naive SHIP-1−/− T cells were less responsive to TCR stimulation, although SHIP-1−/− APC might have increased activity.
SHIP-1 knockout (SHIP-1−/−) mice on BALB/c background were immunized with ovalbumin (OVA) plus aluminum hydroxide, a strong Th2-inducing immunization, and challenged with OVA.
These results indicate that SHIP-1−/− T cells had impaired response to antigen stimulation while SHIP-1−/− APC had enhanced activity in the presence of antigen.
In this study, we examined the role of SHIP-1 in adaptive immune response using SHIP-1 null mice in an allergic asthma model.
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