Q: Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.
Context: Although allergic sensitization can be generated against various allergens, it is unknown how such a diversity of antigens is able to promote TH2-mediated inflammation leading to atopy. Our previous studies demonstrated that allergen-specific IgG immune complexes (ICs) and house dust mite (HDM) extract both induced dendritic cells (DCs) to drive TH2-mediated inflammation, but the mechanism by which these diverse stimuli produce similar responses is unknown.', 'We sought to identify the DC signaling pathways used by TH2 stimuli to promote TH2-mediated inflammation.', 'C57BL/6, FcRIII(-/-), FcR(-/-), and ST2(-/-) mice were sensitized and challenged with HDM, and inflammation was assessed based on results of flow cytometry and histology and cytokine production. Bone marrow-derived DCs from these strains were used in signaling and adoptive transfer experiments.', 'Our findings indicate that 2 distinct TH2 stimuli, ICs and HDM, use the FcR-associated receptors FcRIII and Dectin-2, respectively, to promote TH2-mediated lung inflammation. In this study we demonstrate that both ICs and HDM induce expression of IL-33, a critical mediator in asthma pathogenesis and the differentiation of TH2 cells, in DCs. Upregulation of IL-33 in DCs is dependent on FcR, Toll-like receptor 4, and phosphoinositide 3-kinase. Exogenous IL-33 is sufficient to restore the development of TH2 responses in FcR-deficient mice. Finally, adoptive transfer of allergen-pulsed FcR(+/-) bone-marrow derived DCs restores the development of TH2-type inflammation in FcR-deficient mice, demonstrating the necessity of this signaling pathway in DCs for allergen-induced inflammation.
Answer: These data identify a mechanism whereby TH2 stimuli signal through FcR-associated receptors on DCs to upregulate IL-33 production and induce TH2-mediated allergicairway inflammation.
A:
Does signaling through FcR-associated receptors on dendritic cells drive IL-33-dependent TH2-type responses?