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The role of competition and cooperation in relation to the goal of health equity is examined in this paper. The authors explain why the win-lose mentality associated with avoidable competition is ethically questionable and less effective than cooperation in achieving positive outcomes, particularly as it relates to health and health equity. Competition, which differentiates winners from losers, often with the winner-takes-all reward system, inevitably leads to a few winners and many losers, resulting in social inequality, which, in turn, engenders and perpetuates health inequity.Competitive market-driven approaches to healthcare-brought about by capitalism, neo-liberalization, and globalization, based primarily on a competitive framework-are shown to have contributed to growing inequities with respect to the social determinants of health, and have undermined equal opportunity to access health care and achieve health equity. It is possible to redistribute income and wealth to reduce social inequality, but globalization poses increasing challenges to policy makers. John Stuart Mill provided a passionate, philosophical defense of cooperatives, followed by Karl Polanyi who offered an insightful critique of both state socialism and especially the self-regulating market, thereby opening up the cooperative way of shaping the future. We cite Hannah Arendt's "the banality of evil" to characterize the tragic concept of "ethical fading" witnessed in business and everyday life all over the world, often committed (without thinking and reflecting) by ordinary people under competitive pressures.To promote equity in health for all, we recommend the adoption of a radically new cooperation paradigm, applied whenever possible, to everything in our daily lives.

The mechanisms that regulate the strength and duration of CD8(+) cytotoxic T cell activity determine the effectiveness of an antitumor immune response. To better understand the antitumor effects of anti-cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) antibody treatment, we analyzed the effect of CTLA-4 signaling on CD8(+) T cells in vitro and in vivo. In vitro, cross-linking of CTLA-4 on purified CD8(+) T cells caused decreased proliferative responses to anti-CD3 stimulation and rapid loss of activation marker expression. In vivo, blockade of CTLA-4 by neutralizing anti-CTLA-4 mAb greatly enhanced the accumulation, activation, and cytotoxic activity of CD8(+) T cells induced by immunization with Ag on dendritic cells (DC). This enhanced response did not require the expression of MHC class II molecules on DC or the presence of CD4(+) T cells. These results demonstrate that CTLA-4 blockade is able to directly enhance the proliferation and activation of specific CD8(+) T cells, indicating its potential for tumor immunotherapy even in situations in which CD4(+) T cell help is limited or absent.