This is an extended review essay of the book Radical democracy and collective movements today: The biopolitics of the multitude versus the hegemony of the people. In it, I examine the authors' attempts to synthesize the political theoretical approaches associated with Ernesto Laclau and Antonio Negri, and I argue that such a synthesis can only be an unstable one, since the two approaches operate with incompatible conceptions of ontology.
The idea of 'folklore' has been intensely criticized in recent years. This essay takes these criticisms as its point of departure, offering its own proposal for critically reexamining and reconceptualizing - but not abandoning - the idea of folklore. The author argues that a serious engagement with the idea of 'the folk' can serve as an entry point for understanding the symbolic ambiguity as well as the social significance and political power of what scholars call (or used to call) folklore. Scholars should neither uncritically accept the ideology of the folk, nor hastily banish the idea to the safe realm of the 'emic' as if it had no bearing on the way we as scholars think. If the study of folklore has relevance in today's world, it is above all because of the unusual notion that some kinds of expression are conditioned by some kind of social entity that can be called a folk, which continues to provide the most productive basis for a scholarly discipline studying folklore.
Abstract The cytokines controlling the development of human interleukin (IL) 17--producing T helper cells in vitro have been difficult to identify. We addressed the question of the development of human IL-17--producing T helper cells in vivo by quantifying the production and secretion of IL-17 by fresh T cells ex vivo, and by T cell blasts expanded in vitro from patients with particular genetic traits affecting transforming growth factor (TGF) beta, IL-1, IL-6, or IL-23 responses. Activating mutations in TGFB1, TGFBR1, and TGFBR2 (Camurati-Engelmann disease and Marfan-like syndromes) and loss-of-function mutations in IRAK4 and MYD88 (Mendelian predisposition to pyogenic bacterial infections) had no detectable impact. In contrast, dominant-negative mutations in STAT3 (autosomal-dominant hyperimmunoglobulin E syndrome) and, to a lesser extent, null mutations in IL12B and IL12RB1 (Mendelian susceptibility to mycobacterial diseases) impaired the development of IL-17--producing T cells. These data suggest that IL-12Rbeta1- and STAT-3--dependent signals play a key role in the differentiation and/or expansion of human IL-17-producing T cell populations in vivo. ; The Laboratory of Human Genetics of Infectious Diseases is supported by the Agence Nationale de la Recherche, the Programme Hospitalier de Recherche Clinique, the European Union (grant LHSP-CT-2005-018736), the BNP Paribas Foundation, the March of Dimes, the Dana Foundation, and the Candi'Oser Association. L. de Beaucoudrey is supported by the Fondation pour la Recherche Medicale as part of the PhD program of Pierre et Marie Curie University. J.L. Casanova is an International Scholar of the Howard Hughes Medical Institute.