Understanding Social Class in Place: Responding to Supergentrification in Aspen, Colorado

Existing research portrays elite places as prone to exclusion, welcoming of upscaling, and focused on protecting their economic self-interests. This paper provides nuance to this research by exploring how stakeholders understand and respond to supergentrification. During the fall of 2016, a group of citizen activists in the exclusive community of Aspen, Colorado, initiated an ordinance seeking to limit the expansion of luxury chain stores. Drawing on qualitative data related to this case, we show that how communities respond to supergentrification depends on locally specific understandings of place and social class, and how class interests have been institutionalized in local policies. In Aspen, residents opposed luxury chain stores by marshaling narratives that foreground the community\u27s history of class mixing and the significance of working locals. Elected officials responded by taking account of the political power of local residents as well as the city\u27s dependence on tax revenues from affluent visitors and second homeowners. Our findings extend and complicate understandings of how power works in elite places, highlighting both the potential for, and limitations of, efforts to thwart supergentrification and associated dislocation

Trefoil factor 2 rapidly induces interleukin 33 to promote type 2 immunity during allergic asthma and hookworm infection

The molecular mechanisms that drive mucosal T helper type 2 (T[subscript H]2) responses against parasitic helminths and allergens remain unclear. In this study, we demonstrate in mice that TFF2 (trefoil factor 2), an epithelial cell–derived repair molecule, is needed for the control of lung injury caused by the hookworm parasite Nippostrongylus brasiliensis and for type 2 immunity after infection. TFF2 is also necessary for the rapid production of IL-33, a T[subscript H]2-promoting cytokine, by lung epithelia, alveolar macrophages, and inflammatory dendritic cells in infected mice. TFF2 also increases the severity of allergic lung disease caused by house dust mite antigens or IL-13. Moreover, TFF2 messenger RNA expression is significantly increased in nasal mucosal brushings during asthma exacerbations in children. These experiments extend the biological functions of TFF2 from tissue repair to the initiation and maintenance of mucosal T[subscript H]2 responses