Pandemic payment patterns.

COVID-19 has temporarily changed the relative costs and benefits of different payment methods: cash has become more costly in terms of health risks, ease of use and likelihood of acceptance, whereas debit card usage has become less costly. As a result, consumers have shifted away from cash. Based on unique daily payment diary survey data collected between January 2018 and December 2021 amongst a representative panel of Dutch consumers, we study the shift in payment behaviour and payment preferences during two lockdown periods in the Netherlands in 2020 and 2021. Since the start of the first lockdown the likelihood of debit card usage at the expense of cash has increased by 12 percentage points compared to its trend level. About 60 percent of this shift on top of the autonomous trend persisted several months after the end of the first lockdown and part of it has persisted several months after the end of the second lockdown. The results indicate that the pandemic accelerated the increased usage of debit card at the POS, especially during the first pandemic year. Also, the pandemic has resulted in a shift in payment preferences towards more contactless payments. Both effects are largest for elderly people.

Has the COVID-19 pandemic affected public trust? Evidence for the US and the Netherlands.

Using two large-scale surveys among households, we examine the drivers of public trust in banks, insurance companies, BigTechs, and other people in the United States and the Netherlands, and analyse whether the COVID-19 pandemic has affected public trust. Our results suggest that the COVID-19 pandemic did not have much effect on trust in financial institutions in the US and the Netherlands. However, trust in BigTechs and trust in other people declined in both countries, especially in the US. Our regression results show that the relationship between respondents' characteristics and (changes in) trust differs across the US and the Netherlands. However, for both countries we find evidence that individuals with poor health have lower levels of trust than healthy people, and that trust among poor-health respondents dropped more during the pandemic. Furthermore, trust in other people is positively related to trust in banks, insurance companies, and BigTechs.

Determinants of Trust in Banks' Payment Services During COVID: An Exploration Using Daily Data.

Trust in banks is key, especially in turbulent times. Using unique daily data for a representative panel of Dutch consumers, we examine to what extent the COVID-crisis has affected trust in banks' payment services. We have the following main findings. First, COVID-19 measures have affected trust in banks' payment services. The first lockdown increased narrow-scope trust (trust in consumers' own bank payment services) and broad-scope trust (trust in banks' payment services in general). The second lockdown decreased both notions of trust. The crisis measures impacted the trust of the elderly the strongest. Second, personal characteristics are significantly related to trust in banks' payment services. For example, we find that both types of trust are increasing with digital literacy and the ease of getting by with income. Third, narrow-scope trust is higher than broad-scope trust. The gap between trust in the own bank and trust in banks in general is highest for customers of small banks.

Recruitment of Rab27a to phagosomes controls microbial antigen cross-presentation by dendritic cells.

Polyreactive immunoglobulins (Ig) and complement components are present in tissues and blood of healthy individuals. They facilitate pathogen uptake and inactivation in lysosomes of phagocytes and thereby provide rapid protection against infection. Dendritic cells (DCs) are phagocytes that can acquire peptides from phagocytosed antigen to elicit cytotoxic immune responses by CD8(+) T lymphocytes. The mechanisms that select peptides for cross-presentation are not fully resolved. Here we investigated the role of polyreactive Ig and complement in directing phagosomal antigen processing for cross-presentation. Phagocytosis facilitated by serum opsonization required the presence of Ig for effective antigen cross-presentation of microbe-derived antigen. The presence of complement C3 in serum promoted phagocytosis, yet phagosomes were defective in antigen degradation. The small GTPase Rab27a was recently implicated in antigen cross-presentation and was rapidly recruited to phagosomes only when Ig was present. Our data suggest that prebinding of antigen by polyreactive Ig potentiates the efficiency of antigen cross-presentation to CD8(+) T cells through recruitment of Rab27a.

Mps1 phosphorylates Borealin to control Aurora B activity and chromosome alignment.

Maintenance of chromosomal stability relies on coordination between various processes that are critical for proper chromosome segregation in mitosis. Here we show that monopolar spindle 1 (Mps1) kinase, which is essential for the mitotic checkpoint, also controls correction of improper chromosome attachments. We report that Borealin/DasraB, a member of the complex that regulates the Aurora B kinase, is directly phosphorylated by Mps1 on residues that are crucial for Aurora B activity and chromosome alignment. As a result, cells lacking Mps1 kinase activity fail to efficiently align chromosomes due to impaired Aurora B function at centromeres, leaving improper attachments uncorrected. Strikingly, Borealin/DasraB bearing phosphomimetic mutations restores Aurora B activity and alignment in Mps1-depleted cells. Mps1 thus coordinates attachment error correction and checkpoint signaling, two crucial responses to unproductive chromosome attachments.

The chromosomal passenger complex controls spindle checkpoint function independent from its role in correcting microtubule kinetochore interactions.

The chromosomal passenger complex (CPC) is a critical regulator of chromosome segregation during mitosis by correcting nonbipolar microtubule-kinetochore interactions. By severing these interactions, the CPC is thought to create unattached kinetochores that are subsequently sensed by the spindle assembly checkpoint (SAC) to prevent premature mitotic exit. We now show that spindle checkpoint function of the CPC and its role in eliminating nonbipolar attachments can be uncoupled. Replacing the chromosomal passenger protein INCENP with a mutant allele that lacks its coiled-coil domain results in an overt defect in a SAC-mediated mitotic arrest in response to taxol treatment, indicating that this domain is critical for CPC function in spindle checkpoint control. Surprisingly, this mutant could restore alignment and cytokinesis during unperturbed cell divisions and was capable of resolving syntelic attachments. Also, Aurora-B kinase was localized and activated normally on centromeres in these cells, ruling out a role for the coiled-coil domain in general Aurora-B activation. Thus, mere microtubule destabilization of nonbipolar attachments by the CPC is insufficient to install a checkpoint-dependent mitotic arrest, and additional, microtubule destabilization-independent CPC signaling toward the spindle assembly checkpoint is required for this arrest, potentially through amplification of the unattached kinetochore-derived checkpoint signal.

Regulated expression of the inhibitory receptor LAIR-1 on human peripheral T cells during T cell activation and differentiation.

The leukocyte-associated Ig-like receptor-1 (LAIR-1) is capable of inhibiting immune cell function through interaction with collagens. LAIR is expressed on the majority of peripheral blood mononuclear cells. The abundant expression of both receptor and ligand calls for regulatory mechanisms to relieve the continuous interaction between collagens and LAIR-1. This regulation may occur at the expression level of the receptor. Here, we report that LAIR-1 is indeed differentially expressed during human T cell differentiation. Naive CD4(+) and CD8(+) T cells as well as CD8(+) T cells of the effector phenotype express higher levels of LAIR-1 compared to memory T cells. In vitro stimulation revealed a decrease in LAIR-1 expression upon activation, and the lower LAIR-1 expression on CD127(-) T cells suggests that activation-induced down-modulation of LAIR-1 may also occur in vivo. Furthermore, crosslinking of LAIR-1 on primary T cells results in an inhibition of T cell function. Our data suggest that regulated expression of LAIR-1 and the subsequent change in the threshold for activation may be a mechanism to modulate inhibition of the immune system.