Distribuirani obrambeni mehanizmi za clone napade temeljeni na algoritmu za istraživanje gravitacije (GSA) u WSN

Wireless Sensor Networks (WSN) are often deployed in hostile environment and are vulnerable to attacks because of the resource constrained nature of the sensors. Clone attack in WSN is one of the major issues where the messages are eavesdropped, the captured node is cloned, and multiple nodes with same identity are produced by attacker. In order to overcome these issues, in this paper, a Distributed Defense Mechanism for Clone Attacks based on Gravitational Search Algorithm (GSA) in WSN is proposed. For efficiently detecting the suspect nodes, the nodes in the channel can be divided into witness node and the claimer node. The witness nodes are responsible for the suspect nodes detection, whereas the claimer nodes should provide their identities for the detection process. For the witness nodes selection, we utilize the GSA to pick out the best witness nodes set. After selecting the witness nodes, clone attack detection is performed by observing the behavior of the neighbor nodes. On detecting the clone attack, revocation procedure is triggered to revoke the clone attack in the witness nodes. By simulation results, it can be concluded that the proposed algorithm provides better protection to clone attacks by reducing the packet drop and increasing the packet delivery ratio.Bežične senzorske mreže (WSN) često su raspoređene u neprijateljskom okruženju i ranjive su na napade zbog prirode senzora koji su tehnološki ograničeni. Clone napad u WSN jedan je od glavnih problema gdje se poruke prisluškuju, zarobljeni čvor se klonira te napadač proizvede višestruke čvorove istog identiteta. Kako bi nadvladali te probleme, ovaj rad predlaže distribuirani obrambeni mehanizam za clone napade temeljen na algoritmu za istraživanje gravitacije (GSA) u WSN. Kako bi se sumnjivi čvorovi efikasno detektirali, čvorovi u kanalu mogu se podijeliti u čvorove svjedoke i tražene čvorove. Čvorovi svjedoci odgovorni su za otkrivanje sumnjivih čvorova, dok traženi čvorovi trebaju za potrebe procesa detekcije navesti svoj identitet. Za izbor čvorova svjedoka, koristi se GSA kako bi se izabrala grupa čvorova koji su najprikladniji. Nakon izbora čvorova svjedoka, otkivanje clone napada vrši se promatranjem ponašanja susjednih čvorova. Otkrivanjem clone napada aktivira se proces opoziva kako bi se opozvao clone napad u čvorovima svjedocima. Prema rezultatima dobivenim iz simulacije može se zaključiti kako predloženi algoritam pruža bolju zaštitu od clone napada smanjivanjem odbacivanja paketa i povećavanjem omjera isporuke paketa

Tuning of antigen sensitivity by T cell receptor-dependent negative feedback controls T cell effector function inflammed tissues

Activated T cells must mediate effector responses sufficient to clear pathogens while avoiding excessive tissue damage. Here we have combined dynamic intravital microscopy with ex vivo assessments of T cell cytokine responses to generate a detailed spatiotemporal picture of CD4+ T cell effector regulation in the skin. In response to antigen, effector T cells arrested transiently on antigen presenting cells, briefly producing cytokine and then resuming migration. Antigen recognition led to PD-1 upregulation of the programmed death-1 (PD-1) glycoprotein by T cells and blocking its canonical ligand, programmed death-ligand 1 (PD-L1), lengthened the duration of migration arrest and cytokine production, showing that PD-1 interaction with PD-L1 is a major negative feedback regulator of antigen responsiveness. We speculate that the immune system employs a mechanism involving T cell recruitment, transient activation, and rapid desensitization, allowing the T cell response to rapidly adjust to changes in antigen presentation and minimize collateral injury to the host

The Challenges in SDN/ML Based Network Security : A Survey

Machine Learning is gaining popularity in the network security domain as many more network-enabled devices get connected, as malicious activities become stealthier, and as new technologies like Software Defined Networking (SDN) emerge. Sitting at the application layer and communicating with the control layer, machine learning based SDN security models exercise a huge influence on the routing/switching of the entire SDN. Compromising the models is consequently a very desirable goal. Previous surveys have been done on either adversarial machine learning or the general vulnerabilities of SDNs but not both. Through examination of the latest ML-based SDN security applications and a good look at ML/SDN specific vulnerabilities accompanied by common attack methods on ML, this paper serves as a unique survey, making a case for more secure development processes of ML-based SDN security applications.Comment: 8 pages. arXiv admin note: substantial text overlap with arXiv:1705.0056

Retrieving Infinite Numbers of Patterns in a Spin-Glass Model of Immune Networks

The similarity between neural and immune networks has been known for decades, but so far we did not understand the mechanism that allows the immune system, unlike associative neural networks, to recall and execute a large number of memorized defense strategies {\em in parallel}. The explanation turns out to lie in the network topology. Neurons interact typically with a large number of other neurons, whereas interactions among lymphocytes in immune networks are very specific, and described by graphs with finite connectivity. In this paper we use replica techniques to solve a statistical mechanical immune network model with `coordinator branches' (T-cells) and `effector branches' (B-cells), and show how the finite connectivity enables the system to manage an extensive number of immune clones simultaneously, even above the percolation threshold. The system exhibits only weak ergodicity breaking, so that both multiple antigen defense and homeostasis can be accomplished.Comment: Editor's Choice 201

An Early Reduction in Treg Cells Correlates with Enhanced Local Inflammation in Cutaneous Leishmaniasis in CCR6-Deficient Mice

Resistance to Leishmania major infection is dependent on the development of a cell-mediated Th1 immune response in resistant C57BL/6 mice whereas Th2-prone BALB/c mice develop non-healing lesions after infection. The chemokine receptor CCR6 is shared by anti-inflammatory regulatory T cells and pro-inflammatory Th17 cells. In a recent study we showed that C57BL/6 mice deficient in CCR6 exhibited enhanced footpad swelling and impaired T helper cell migration indicated by reduced recruitment of total T helper cells into the skin after infection and a reduced delayed type hypersensitivity reaction. Based on these findings we tested whether the lack of CCR6 alters Treg or Th17 cell responses during the course of Leishmania major infection. When we analyzed T cell subsets in the lymph nodes of CCR6-deficient mice, Th17 cell numbers were not different. However, reduced numbers of Treg cells paralleled with a stronger IFNγ response. Furthermore, the early increase in IFNγ-producing cells correlated with increased local tissue inflammation at later time points. Our data indicate an important role of CCR6 for Treg cells and a redundant role for Th17 cells in a Th1 cell-driven anti-parasitic immune response against Leishmania major parasites in resistant C57BL/6 mice

Reciprocal expression of interferon gamma or interleukin 4 during the resolution or progression of murine leishmaniasis. Evidence for expansion of distinct helper T cell subsets.

We purified poly(A)+ mRNA from the spleen and lymph nodes at designated times after infection with Leishmania major in genetically susceptible BALB/c and resistant C57BL/6 mice. The steady-state levels of IL-2, IFN-gamma, IL-4, and IL-1 beta mRNA were determined using Northern hybridizations. IL-2 mRNA levels in the infected organs of BALB/c and C57BL/6 mice were comparable after infection, but IFN-gamma and IL-4 mRNA levels were reciprocally expressed. Levels of IFN-gamma mRNA in C57BL/6 draining nodes and spleen were significantly greater than in BALB/c mice except at 4 and 6 wk of infection, when splenic IFN-gamma mRNA levels were transiently comparable. In contrast, IL-4 mRNA was apparent only in BALB/c and not in C57BL/6 nodes and spleen. Tissue levels of IL-1 beta mRNA were 10-20-fold greater in BALB/c mice. BALB/c mice were pretreated with GK1.5 mAb, a manipulation that promotes healing of subsequent infection by transiently depleting L3T4+ cells. At 8 wk of infection, by which time lymphoid organs were repopulated with L3T4+ cells, GK1.5-pretreated BALB/c mice produced IFN-gamma, but not IL-4 message. Serum levels of IgE were markedly elevated in infected BALB/c, but not in infected C57BL/6 or GK1.5-pretreated BALB/c mice, consistent with in vivo biologic activity of IL-4 in nonhealing mice. Treatment of infected BALB/c mice with neutralizing anti-IL-4 antibody abolished the elevation of serum IgE and significantly attenuated the progression of disease as assessed by size and ulceration of the lesion, and by reduction in the number of tissue parasites. Both protective and deleterious responses to Leishmania infection have previously been shown to be L3T4+ cell dependent. Our findings are consistent with the differential expansion of protective, IFN-gamma-producing Th1 cells in healing mice, and the expansion of deleterious, IL-4-producing Th2 cells in nonhealing mice. The inverse relationship of IFN-gamma and IL-4 gene expression during leishmaniasis may underlie the divergence of cellular and humoral immunity that occurs during chronic infection with Leishmania and possibly other intracellular parasites

Interleukin-17 is required for control of chronic lung infection caused by Pseudomonas aeruginosa

Chronic pulmonary infection with Pseudomonas aeruginosa is a feature of cystic fibrosis (CF) and other chronic lung diseases. Cytokines of the IL-17 family have been proposed as important in the host response to P. aeruginosa infection through augmenting antibacterial immune responses, although their pro-inflammatory effect may contribute to lung damage that occurs as a result of chronic infection. We set out to explore the role of IL-17 in the host response to chronic P. aeruginosa infection. We used a murine model of chronic pulmonary infection with CF-related strains of P. aeruginosa. We demonstrate that IL-17 cytokine signaling is essential for survival and prevention of chronic infection at 2 weeks post-inoculation using two different P. aeruginosa strains. Following infection, there was a marked expansion of cells within mediastinal lymph nodes, comprised mainly of innate lymphoid cells (ILCs); ∼90% of IL-17 producing cells had markers consistent with Group 3 ILCs. A smaller percentage of IL-17+ cells had markers consistent with a B1 phenotype. In lung homogenates 14 days following infection, there was a significant expansion of IL-17+ cells – about 50% of these were CD3+, split equally between CD4+ Th17 cells and γδ T cells, while the CD3- IL-17+ cells were almost exclusively Group 3 ILCs. Further experiments with B cell deficient mice showed that B cell production of IL-17 or natural antibodies did not provide any defence against chronic P. aeruginosa infection. Thus, IL-17 rather than antibody is a key element in host defence against chronic pulmonary infection with P. aeruginosa