Towards a realistic microscopic description of highway traffic

Simple cellular automata models are able to reproduce the basic properties of highway traffic. The comparison with empirical data for microscopic quantities requires a more detailed description of the elementary dynamics. Based on existing cellular automata models we propose an improved discrete model incorporating anticipation effects, reduced acceleration capabilities and an enhanced interaction horizon for braking. The modified model is able to reproduce the three phases (free-flow, synchronized, and stop-and-go) observed in real traffic. Furthermore we find a good agreement with detailed empirical single-vehicle data in all phases.Comment: 7 pages, 7 figure

An empirical test for cellular automaton models of traffic flow

Based on a detailed microscopic test scenario motivated by recent empirical studies of single-vehicle data, several cellular automaton models for traffic flow are compared. We find three levels of agreement with the empirical data: 1) models that do not reproduce even qualitatively the most important empirical observations, 2) models that are on a macroscopic level in reasonable agreement with the empirics, and 3) models that reproduce the empirical data on a microscopic level as well. Our results are not only relevant for applications, but also shed new light on the relevant interactions in traffic flow.Comment: 28 pages, 36 figures, accepted for publication in PR

Adaptive NK cells in people exposed to Plasmodium falciparum correlate with protection from malaria

How antibodies naturally acquired during Plasmodium falciparum infection provide clinical immunity to blood-stage malaria is unclear. We studied the function of natural killer (NK) cells in people living in a malaria-endemic region of Mali. Multi-parameter flow cytometry revealed a high proportion of adaptive NK cells, which are defined by the loss of transcription factor PLZF and Fc receptor γ-chain. Adaptive NK cells dominated antibody-dependent cellular cytotoxicity responses, and their frequency within total NK cells correlated with lower parasitemia and resistance to malaria. P. falciparum–infected RBCs induced NK cell degranulation after addition of plasma from malaria-resistant individuals. Malaria-susceptible subjects with the largest increase in PLZF-negative NK cells during the transmission season had improved odds of resistance during the subsequent season. Thus, antibody-dependent lysis of P. falciparum–infected RBCs by NK cells may be a mechanism of acquired immunity to malaria. Consideration of antibody-dependent NK cell responses to P. falciparum antigens is therefore warranted in the design of malaria vaccines

Variations in killer-cell immunoglobulin-like receptor and human leukocyte antigen genes and immunity to malaria

Malaria is one of the deadliest infectious diseases in the world. Immune responses to Plasmodium falciparum malaria vary among individuals and between populations. Human genetic variation in immune system genes is likely to play a role in this heterogeneity. Natural killer (NK) cells produce inflammatory cytokines in response to malaria infection, kill intraerythrocytic Plasmodium falciparum parasites by cytolysis, and participate in the initiation and development of adaptive immune responses to plasmodial infection. These functions are modulated by interactions between killer-cell immunoglobulin-like receptors (KIR) and human leukocyte antigens (HLA). Therefore, variations in KIR and HLA genes can have a direct impact on NK cell functions. Understanding the role of KIR and HLA in immunity to malaria can help to better characterize antimalarial immune responses. In this review, we summarize the different KIR and HLA so far associated with immunity to malaria.This work was supported through the DELTAS Africa Initiative (Grant no. 107743), that funded Stephen Tukwasibwe through PhD fellowship award, and Annettee Nakimuli through group leader award. The DELTAS Africa Initiative is an independent funding scheme of the African Academy of Science (AAS), Alliance for Accelerating Excellence in Science in Africa (AESA) and supported by the New Partnership for Africa’s Development Planning and Coordinating Agency (NEPAD Agency) with funding from the Wellcome Trust (Grant no. 107743) and the UK government. Francesco Colucci is funded by Wellcome Trust grant 200841/Z/16/Z. The project received funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (grant agreement No. 695551) for James Traherne and John Trowsdale. Jyothi Jayaraman is a recipient of fellowship from the Centre for Trophoblast Research

Cytokines regulate the antigen-presenting characteristics of human circulating and tissue-resident intestinal ILCs

ILCs and T helper cells have been shown to exert bi-directional regulation in mice. However, how crosstalk between ILCs and CD4(+) T cells influences immune function in humans is unknown. Here we show that human intestinal ILCs co-localize with T cells in healthy and colorectal cancer tissue and display elevated HLA-DR expression in tumor and tumor-adjacent areas. Although mostly lacking co-stimulatory molecules ex vivo, intestinal and peripheral blood (PB) ILCs acquire antigen-presenting characteristics triggered by inflammasome-associated cytokines IL-1 beta and IL-18. IL-1 beta drives the expression of HLA-DR and co-stimulatory molecules on PB ILCs in an NF-kappa B-dependent manner, priming them as efficient inducers of cytomegalovirus-specific memory CD4(+) T-cell responses. This effect is strongly inhibited by the anti-inflammatory cytokine TGF-beta. Our results suggest that circulating and tissue-resident ILCs have the intrinsic capacity to respond to the immediate cytokine milieu and regulate local CD4(+) T-cell responses, with potential implications for anti-tumor immunity and inflammation. Murine ILCs can modulate T cell responses in MHCII-dependent manner. Here the authors show that human ILCs process and present antigens and induce T-cell responses upon exposure to IL-1-family cytokines; along with the article by Lehmann et al, this work elucidates how cytokines set context specificity of ILC-T cell crosstalk by regulating ILC antigen presentation.Funding Agencies|Knut and Alice Wallenberg FoundationKnut &amp; Alice Wallenberg Foundation; Swedish Research CouncilSwedish Research Council; Centre for Innovative Medicine; Jonasson center at the Royal Institute of Technology, Sweden; board of research at the Karolinska InstituteKarolinska Institutet; research committee at the Karolinska hospital; German Research Foundation (Deutsche Forschungsgemeinschaft)German Research Foundation (DFG) [RA 2986/1-1]; Swedish Cancer Foundation [130396, 160664, 170082]; Swedish Research CouncilSwedish Research Council [521-2013-2791]; Swedish Society for Medical Research [4-140/2014]; Swedish Foundation for Strategic ResearchSwedish Foundation for Strategic Research [FFL15-0120]; Knut and Alice Wallenberg FoundationKnut &amp; Alice Wallenberg Foundation [4-1198/2016]; EMBO long-term fellowshipEuropean Molecular Biology Organization (EMBO) [ALTF 786-2013]; Karolinska InstitutetKarolinska Institutet; ERC-2013-ADG [341038]</p