Estimating Attendance From Cellular Network Data

We present a methodology to estimate the number of attendees to events happening in the city from cellular network data. In this work we used anonymized Call Detail Records (CDRs) comprising data on where and when users access the cellular network. Our approach is based on two key ideas: (1) we identify the network cells associated to the event location. (2) We verify the attendance of each user, as a measure of whether (s)he generates CDRs during the event, but not during other times. We evaluate our approach to estimate the number of attendees to a number of events ranging from football matches in stadiums to concerts and festivals in open squares. Comparing our results with the best groundtruth data available, our estimates provide a median error of less than 15% of the actual number of attendees

Automatic identification of relevant places from cellular network data

We present a methodology to automatically identify users\u2019 relevant places from cellular network data.1 In this work we used anonymized Call Detail Record (CDR) comprising information on where and when users access the cellular network. The key idea is to effectively cluster CDRs together and to weigh clusters to determine those associated to frequented places. The approach can identify users\u2019 home and work locations as well as other places (e.g., associated to leisure and night life). We evaluated our approach threefold: (i) on the basis of groundtruth information coming from a fraction of users whose relevant places were known, (ii) by comparing the resulting number of inhabitants of a given city with the number of inhabitants as extracted by the national census. (iii) Via stability analysis to verify the consistency of the extracted results across multiple time periods. Results show the effectiveness of our approach with an average 90% precision and recall

IL-34 deficiency impairs FOXP3+ Treg function in a model of autoimmune colitis and decreases immune tolerance homeostasis

BACKGROUND: Immune homeostasis requires fully functional Tregs with a stable phenotype to control autoimmunity. Although IL-34 is a cytokine first described as mainly involved in monocyte cell survival and differentiation, we recently described its expression by CD8 METHODS: We generated Il34 RESULTS: Here we report that the absence of expression of IL-34 in Il34 CONCLUSION: Altogether, our data emphasize on the crucial necessity of IL-34 for immune homeostasis and for CD4 HIGHLIGHTS: -Absence of expression of IL-34 in Il3

IL-15 sustains IL-7R-independent ILC2 and ILC3 development

The signals that maintain tissue-resident innate lymphoid cells (ILC) in different microenvironments are incompletely understood. Here we show that IL-7 receptor (IL-7R) is not strictly required for the development of any ILC subset, as residual cells persist in the small intestinal lamina propria (siLP) of adult and neonatal Il7ra(−/−) mice. Il7ra(−/−) ILC2 primarily express an ST2(−) phenotype, but are not inflammatory ILC2. CCR6(+) ILC3, which express higher Bcl-2 than other ILC3, are the most abundant subset in Il7ra(−/−) siLP. All ILC subsets are functionally competent in vitro, and are sufficient to provide enhanced protection to infection with C. rodentium. IL-15 equally sustains wild-type and Il7ra(−/−) ILC survival in vitro and compensates for IL-7R deficiency, as residual ILCs are depleted in mice lacking both molecules. Collectively, these data demonstrate that siLP ILCs are not completely IL-7R dependent, but can persist partially through IL-15 signalling

AHR and the Transcriptional Regulation of Type-17/22 ILC

Mucosal innate lymphoid cells (ILCs) are an emerging population of diverse and heterogeneous immune cells, all with the unique ability to mount a rapid response against invading pathogens. They are further divided into subsets based on their differing cell surface markers as well as in their functional specialization. In this review, we summarize recent reports describing the importance of the transcription factor aryl hydrocarbon receptor (AHR) in regulating the development of one of these subsets, the Type-17/22 ILCs, as well as in the organization of postnatal lymphoid structures. We discuss the mechanisms behind the AHR dependence for development in Type-17/22 ILCs as well as reviewing the proposed physiological ligands that are mediating this effect