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. Author manuscript; available in PMC: 2008 Dec 1.
Published in final edited form as: Nat Med. 2008 May 18;14(6):633–640. doi: 10.1038/nm1770

Figure 6.

Figure 6

Scheme for an NKT cell-macrophage immune axis leading to chronic airway disease after viral infection. Virus may directly or indirectly facilitate CD1d-dependent antigen presentation and consequent activation of invariant CD4− NKT cells. NKT cells then interact directly with lung macrophages via contact between invariant Vα14 TCR and glycolipid-loaded CD1d. This interaction leads to increased expression of IL-13R and production of IL-13 that drives a positive feedback loop to amplify IL-13 production and alternative activation of macrophages, including Chi3l3/4, Fizz1, Mmp12, Arg1, and Alox12e gene expression. Persistent IL-13 production also drives differentiation of airway epithelial cell precursors towards mucous cells (mucous cell metaplasia) and airway smooth muscle cells to become more reactive to contractile agonists (airway hyperreactivity or AHR).