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This article investigates attitudes towards the conditionality of benefits targeted to a specific needy group, the unemployed, and analyses their relationship with the structure of income inequality. The focus is on the deservingness of welfare recipients. The public seems to use five criteria to define deservingness and, consequently, the conditionality to which public support is subjected: need, attitude (i.e. gratefulness), control (over neediness), reciprocity (of giving and receiving) and identity, that is the similarity or proximity between the providers of public support (the taxpayers) and the people who should receive it. People’s willingness to help depends on how close they consider benefit recipients to be to themselves (i.e. the extent to which they belong to the same in-group). The identity criterion is the main object of our investigation. We argue that the operation of this criterion at the micro-level can be affected by macro-level variables. Specifically, we focus on different measures of the structure of income inequality which are indicators of the social distance between welfare recipients and taxpayers. Based on data from three waves of the European Values Study (1990–2008) collected in 30 countries, the study offers a comparative and longitudinal analysis. The picture emerging from the within-country analysis – which removed much of the between-country heterogeneity − shows that when the social distance grows, it is more difficult for the majority of citizens (upper and middle classes) to identify with the unemployed.

The tetraspan surface molecule MS4A4A is selectively expressed by cells of the monocyte-macrophage lineage(s), being induced during monocyte-to-macrophage differentiation, but not in dendritic cells. In vitro, MS4A4A is upregulated in macrophages by M2 or M2-like signals, including IL-4 and dexamethasone. In vivo, MS4A4A is expressed by human tissue resident macrophages, macrophages infiltrating the inflamed synovium in rheumatoid arthritis patients, and tumor-associated macrophages, and is induced in monocytes in patients treated with methylprednisolone. After macrophage engagement with Zymosan, an agonist of β-glucan receptor Dectin-1, MS4A4A colocalizes with Dectin-1 in the lipid rafts. In the absence of MS4A4A, activation of the Syk pathway downstream Dectin-1 is impaired, and the production of cytokines and reactive oxygen species is reduced. MS4A4A deficiency in macrophages has no impact on primary tumor growth, but compromises Dectin-1-driven NK cell-mediated resistance to metastasis. Thus, MS4A4A is a tetraspan molecule expressed during macrophage differentiation and M2/M2-like polarization that functionally interacts with Dectin-1 and is essential for full response by this innate immunity receptor, including NK cell-mediated resistance to metastasis.

As a consequence of the rising number of dual-earner households, many contemporary couples in europe face two potentially conflicting job schedules when figuring out how to allocate their time over a week. In this article, we study how dual-earner couples with children organize their working time in belgium, italy, and the netherlands. We place working time coordination explicitly in a comparative framework to allow cross-country differences in time-scheduling mechanisms to be revealed. We define working time coordination as an act that leads to hours of paid work performed by both parents at the same moment and of which the joint nature cannot be explained by factors other than the partners’ potential to communicate on the timing of their work. Our main findings are as follows: (1) parents actively coordinate their working times in all three societies; (2) on average, italian and flemish dual-earner parents tend to synchronize (increase their work-time overlap), which indicates that parents aim at spending non-market time jointly; and (3) dutch dual-earner parents tend to de-synchronize (decrease work-time overlap), which indicates that the latter tend to maximize the amount of time that at least one parent is out of the job.

CRISPR/Cas9 has become a powerful method to engineer genomes and to activate or to repress genes expression. As such, in cancer research CRISPR/Cas9 technology represents an efficient tool to dissect mechanisms of tumorigenesis and to discover novel targets for drug development. Here, we employed the CRISPR/Cas9 technology for studying the role of prostaglandin-endoperoxide synthase 2 (PTGS2) in melanoma development and progression. Melanoma is the most aggressive form of skin cancer with a median survival of less than 1 year. Although oncogene-targeted drugs and immune checkpoint inhibitors have demonstrated a significant success in improving overall survival in patients, related toxicity and emerging resistance are ongoing challenges. Gene therapy appears to be an appealing option to enhance the efficacy of currently available melanoma therapeutics leading to better patient prognosis. Several gene therapy targets have been identified and have proven to be effective against melanoma cells. Particularly, PTGS2 is frequently expressed in malignant melanomas and its expression significantly correlates with poor survival in patients. In this study we investigated on the effect of ptgs2 knockdown in B16F10 murine melanoma cells. Our results show that reduced expression of ptgs2 in melanoma cells: i) inhibits cell proliferation, migration, and invasiveness; ii) modulates immune response by impairing myeloid derived suppressor cell differentiation; iii) reduces tumor development and metastasis in vivo. Collectively, these findings indicate that ptgs2 could represent an ideal gene to be targeted to improve success rates in the development of new and highly selective drugs for melanoma treatment.

Summary Neutrophils are a component of the tumor microenvironment and have been predominantly associated with cancer progression. Using a genetic approach complemented by adoptive transfer, we found that neutrophils are essential for resistance against primary 3-methylcholantrene-induced carcinogenesis. Neutrophils were essential for the activation of an interferon-γ-dependent pathway of immune resistance, associated with polarization of a subset of CD4− CD8− unconventional αβ T cells (UTCαβ). Bulk and single-cell RNA sequencing (scRNA-seq) analyses unveiled the innate-like features and diversity of UTCαβ associated with neutrophil-dependent anti-sarcoma immunity. In selected human tumors, including undifferentiated pleomorphic sarcoma, CSF3R expression, a neutrophil signature and neutrophil infiltration were associated with a type 1 immune response and better clinical outcome. Thus, neutrophils driving UTCαβ polarization and type 1 immunity are essential for resistance against murine sarcomas and selected human tumors., Graphical Abstract, Highlights • Neutrophils mediate antitumor response by sustaining an IL-12/IFNγ-dependent pathway • Neutrophils are essential for unconventional αβ T cell (UTCαβ) type 1 polarization • Type 1 UTCαβ possess an innate-like phenotype and display antitumor potential in vivo • Neutrophil infiltration is associated with good prognosis in selected human tumors, Tumor-associated neutrophils (TANs) have mainly been portrayed as tumor-promoters. Here, we describe a novel antitumor pathway in which TANs promote IL-12 production by macrophages, leading to type 1 polarization of a subset of unconventional αβ T cell (UTCαβ). Type 1 UTCαβ possess an innate-like phenotype and antitumor potential in vivo. In selected human tumors, neutrophil infiltration is associated with type 1 immunity and better clinical outcome.

Chronic inflammation, including that driven by autoimmunity, is associated with the development of B-cell lymphomas. IL1R8 is a regulatory receptor belonging to the IL1R family, which negatively regulates NF-κB activation following stimulation of IL1R or Toll-like receptor family members. IL1R8 deficiency is associated with the development of severe autoimmune lupus-like disease in lpr mice. We herein investigated whether concomitant exacerbated inflammation and autoimmunity caused by the deficiency of IL1R8 could recapitulate autoimmunity-associated lymphomagenesis. We thus monitored B-cell lymphoma development during the aging of IL1R8-deficient lpr mice, observing an increased lymphoid cell expansion that evolved to diffuse large B-cell lymphoma (DLBCL). Molecular and gene-expression analyses showed that the NF-κB pathway was constitutively activated in Il1r8−/−/lpr B splenocytes. In human DLBCL, IL1R8 had reduced expression compared with normal B cells, and higher IL1R8 expression was associated with a better outcome. Thus, IL1R8 silencing is associated with increased lymphoproliferation and transformation in the pathogenesis of B-cell lymphomas associated with autoimmunity.