Development aid and international migration to Italy: Does aid reduce irregular flows?

In recent years, donors have claimed to tackle the root causes of migration from low‐income countries using aid. While others have studied the effects of aid on regular migration, we test whether aid deters irregular migration to Italy using two innovative dependent variables: asylum applications and apprehensions at border. For asylum applications, the largest significant effect size implies we should expect one extra application for an additional $162,000 in bilateral aid. For border crossings, the only significant effect implies the marginal cost in bilateral aid is$1.8 million per deterred migrant. The conclusion that effect sizes are small is robust to different types of aid, measures of migration and various controls. We find robust evidence that irregular migration flows are significantly affected by conflict, poverty, and the pre‐existing stocks from that country. Comparing our results to the existing aid‐migration literature, we find similar effect sizes. The cost per deterred (regular) migrant is in the range $4‐7 million. Statistically significant estimates for the effect of aid on regular migration are only found for sub‐samples or specific specifications. In short, aid does not deter regular or irregular migration, so should be used for other purposes

Differential T-cell activation by B7-1 expression

T-cell receptor-mediated T-cell activation requires cosimulation signal, which can be provided by B7-1 molecule. Our previous study demonstrated that the coexpression of a covalent peptide/major histocompatibility complex class II molecule complex and costimulatory molecule B7-1 by recombinant adenovirus leads to synergy in peptide-specific T-cell activation. However, the viral antigen-specific T-cell activation is not enhanced by B7-1 expressed by the adenovirus. To verify the differential T cell activation by B7-1 and investigate its underlying mechanisms, we constructed an adenovirus coexpressing a covalent complex of hen egg lysozyme peptide/I-A(k) (HEL(46–61)/I-A(k)) and B7-1 in the present study. In vivo studies revealed that HEL(46–61)-specific T-cell response, but not viral antigen-specific T-cell response, was enhanced by B7-1 expression mediated by the adenovirus, suggesting that exogenous B7-1 expression may regulate T-cell response to these two different antigens through distinct mechanisms. Furthermore, our results revealed that antigen-presenting cells were unsusceptible to adenovirus infection in vivo. Based on these findings, the possible mechanism of differential B7-1 costimulation on peptide-specific and viral antigen-specific T-cell activation is discussed