Transplant arteriosclerosis (TA) is the hallmark of chronic allograft dysfunction (CAD) affecting transplanted organs in the long term [1,2]. These fibroproliferative lesions lead to neointimal thickening of arteries in all transplanted allografts [2]. Luminal narrowing then leads to graft ischemia and organ demise. To date, there are no known tolerance induction strategies that prevent TA [3,4]. Therefore, this study was designed to test the hypothesis that human regulatory T cells (Treg cells) expanded ex vivo could prevent TA. Here we show the comparative capacity of Treg cells, sorted via two separate strategies, to prevent TA in a clinically relevant chimeric humanized mouse system. We found that the in vivo development of TA in human arteries was prevented with the treatment of ex vivo expanded human Treg cells. Additionally, we show that Treg cells sorted based on the low expression of CD127 (IL-7Rα) provide a more potent therapy to conventional Treg cells. Our results demonstrate, for the first time, that human Treg cells can inhibit TA by impairing effector function and graft infiltration. We anticipate our findings to serve as a foundation for the clinical development of therapeutics targeting TA in both allograft transplantation and other immune-mediated causes of vasculopathy [5].
Information-Centric Networking (ICN) has been proposed as one of the future Internet architectures. It is poised to address the challenges faced by today's Internet that include, but not limited to, scalability, addressing, security, and privacy. Furthermore, it also aims at meeting the requirements for new emerging Internet applications. To realize ICN, Named Data Networking (NDN) is one of the recent implementations of ICN that provides a suitable communication approach due to its clean slate design and simple communication model. There are a plethora of applications realized through ICN in different domains where data is the focal point of communication. One such domain is Intelligent Transportation System (ITS) realized through Vehicular Ad hoc NETwork (VANET) where vehicles exchange information and content with each other and with the infrastructure. To date, excellent research results have been yielded in the VANET domain aiming at safe, reliable, and infotainment-rich driving experience. However, due to the dynamic topologies, host-centric model, and ephemeral nature of vehicular communication, various challenges are faced by VANET that hinder the realization of successful vehicular networks and adversely affect the data dissemination, content delivery, and user experiences. To fill these gaps, NDN has been extensively used as underlying communication paradigm for VANET. Inspired by the extensive research results in NDN-based VANET, in this paper, we provide a detailed and systematic review of NDN-driven VANET. More precisely, we investigate the role of NDN in VANET and discuss the feasibility of NDN architecture in VANET environment. Subsequently, we cover in detail, NDN-based naming, routing and forwarding, caching, mobility, and security mechanism for VANET. Furthermore, we discuss the existing standards, solutions, and simulation tools used in NDN-based VANET. Finally, we also identify open challenges and issues faced by NDN-driven VANET and highlight future research directions that should be addressed by the research community.
There is now considerable evidence suggesting that CD8+ T cells are able to generate effector but not functional memory T cells following pathogenic infections in the absence of CD4+ T cells. We show that following transplantation of allogeneic skin, in the absence of CD4+ T cells, CD8+ T cells become activated, proliferate, and expand exclusively in the draining lymph nodes and are able to infiltrate and reject skin allografts. CD44+CD8+ T cells isolated 100 days after transplantation rapidly produce IFN-γ following restimulation with alloantigen in vitro. In vivo CD44+CD8+ T cells rejected donor-type skin allografts more rapidly than naive CD8+ T cells demonstrating the ability of these putative memory T cells to mount an effective recall response in vivo. These data form the first direct demonstration that CD8+ T cells are able to generate memory as well as effector cells in response to alloantigen during rejection in the complete absence of CD4+ T cells. These data have important implications for the design of therapies to combat rejection and serve to reinforce the view that CD8+ T cell responses to allografts require manipulation in addition to CD4+ T cell responses to completely prevent the rejection of foreign organ transplants.
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