105 research outputs found
Racism and hate speech – A critique of Scanlon’s Contractual Theory
The First Amendment is an important value in American liberal polity. Under this value, racism, hate speech and offensive speech are protected speech. This article scrutinizes one of the clear representatives of the American liberal polity - Thomas Scanlon. The paper tracks the developments in his theory over the years. It is argued that Scanlon’s arguments downplay tangible harm that speech might inflict on its target victim audience. Scanlon’s distinction between participant interests, audience interests, and the interests of bystanders is put under close scrutiny. The article criticizes viewpoint neutrality and suggests a balancing approach, further arguing that democracy is required to develop protective mechanisms against harm-facilitating speech as well as profound offences. Both should be taken most seriously
Selective C-Rel Activation via Malt1 Controls Anti-Fungal TH-17 Immunity by Dectin-1 and Dectin-2
C-type lectins dectin-1 and dectin-2 on dendritic cells elicit protective immunity against fungal infections through induction of TH1 and TH-17 cellular responses. Fungal recognition by dectin-1 on human dendritic cells engages the CARD9-Bcl10-Malt1 module to activate NF-κB. Here we demonstrate that Malt1 recruitment is pivotal to TH-17 immunity by selective activation of NF-κB subunit c-Rel, which induces expression of TH-17-polarizing cytokines IL-1β and IL-23p19. Malt1 inhibition abrogates c-Rel activation and TH-17 immunity to Candida species. We found that Malt1-mediated activation of c-Rel is similarly essential to induction of TH-17-polarizing cytokines by dectin-2. Whereas dectin-1 activates all NF-κB subunits, dectin-2 selectively activates c-Rel, signifying a specialized TH-17-enhancing function for dectin-2 in anti-fungal immunity by human dendritic cells. Thus, dectin-1 and dectin-2 control adaptive TH-17 immunity to fungi via Malt1-dependent activation of c-Rel
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