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• W2113493337 abstract "RATIONALE: LILRB4 is an inhibitory receptor that suppresses effector mechanisms of pathologic inflammation driven by mast cell or neutrophil activation. However, it was not known whether LILRB4 inhibits the afferent phase of an immune response and ensuing inflammation. We therefore compared the responses of Lilrb4+/+ and Lilrb4-/- mice in a model of Th2 allergic airway inflammation.METHODS:Lilrb4+/+ and Lilrb4-/- mice were sensitized intranasally with 100 μg of LPS-depleted OVA and 100 ng of LPS in PBS (OVA-LPS) on days 0, 1, and 2. Negative control mice received PBS. On days 14, 15, 18, and 19, mice were challenged intranasally with 25 μg of LPS-depleted OVA. On day 21, BAL, lung, serum, and intrathoracic lymph node cells were obtained. The latter were cultured with 1 mg/ml of LPS-depleted OVA for 72 h.RESULTS: Both Lilrb4+/+ and Lilrb4-/- OVA-LPS mice exhibited significant increases in pulmonary inflammation and Th2 cytokine production by OVA-restimulated lymph node cells, compared with PBS mice. However, Lilrb4-/- OVA-LPS mice demonstrated significantly greater increases in the number of BAL eosinophils and lymphocytes, as well as greater increases in perivascular and peribronchial inflammation, compared with Lilrb4+/+ OVA-LPS mice. OVA-restimulated lymph node cells from Lilrb4-/- mice secreted significantly more IL-4, IL-5, and IL-13 than cells from Lilrb4+/+ animals. In addition, serum levels of OVA-specific IgE and IgG1 were greater in Lilrb4-/- OVA-LPS mice than in Lilrb4+/+ OVA-LPS mice.CONCLUSIONS: Our findings establish that LILRB4 counterregulates the development of Th2 adaptive immune and inflammatory responses in a model of allergic airway inflammation. RATIONALE: LILRB4 is an inhibitory receptor that suppresses effector mechanisms of pathologic inflammation driven by mast cell or neutrophil activation. However, it was not known whether LILRB4 inhibits the afferent phase of an immune response and ensuing inflammation. We therefore compared the responses of Lilrb4+/+ and Lilrb4-/- mice in a model of Th2 allergic airway inflammation. METHODS:Lilrb4+/+ and Lilrb4-/- mice were sensitized intranasally with 100 μg of LPS-depleted OVA and 100 ng of LPS in PBS (OVA-LPS) on days 0, 1, and 2. Negative control mice received PBS. On days 14, 15, 18, and 19, mice were challenged intranasally with 25 μg of LPS-depleted OVA. On day 21, BAL, lung, serum, and intrathoracic lymph node cells were obtained. The latter were cultured with 1 mg/ml of LPS-depleted OVA for 72 h. RESULTS: Both Lilrb4+/+ and Lilrb4-/- OVA-LPS mice exhibited significant increases in pulmonary inflammation and Th2 cytokine production by OVA-restimulated lymph node cells, compared with PBS mice. However, Lilrb4-/- OVA-LPS mice demonstrated significantly greater increases in the number of BAL eosinophils and lymphocytes, as well as greater increases in perivascular and peribronchial inflammation, compared with Lilrb4+/+ OVA-LPS mice. OVA-restimulated lymph node cells from Lilrb4-/- mice secreted significantly more IL-4, IL-5, and IL-13 than cells from Lilrb4+/+ animals. In addition, serum levels of OVA-specific IgE and IgG1 were greater in Lilrb4-/- OVA-LPS mice than in Lilrb4+/+ OVA-LPS mice. CONCLUSIONS: Our findings establish that LILRB4 counterregulates the development of Th2 adaptive immune and inflammatory responses in a model of allergic airway inflammation." @default.
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• W2113493337 date "2007-01-01" @default.
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• W2113493337 title "LILRB4 Suppresses the Development of Th2 Allergic Airway Inflammation" @default.
• W2113493337 doi "https://doi.org/10.1016/j.jaci.2006.11.485" @default.
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