In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

[EX Q]: We live in a hostile environment, surrounded by microbial pathogens and subject to a range of physical and chemical insults. To survive in this environment, vertebrates have evolved complex immune systems. A key element of this defence is the deployment of rapid response elements at the most probable sites of attack, which are the epithelial-cell boundaries between the body and the environment in the skin, gut and lungs. As the body's largest and most exposed interface with the environment, the skin has a central role in host defence. Before the relatively recent discovery of the immunological defences of skin, the cutaneous interface was viewed as a passive barrier between the host and the hostile environment. In the past few decades, however, it has become apparent that the mechanical aspects of epidermal defence are reinforced by a versatile and robust system of immune surveillance 1 (FIG. 1) . The crucial role of immune surveillance in maintaining homeostasis is evident from the marked increase in the frequency and severity of cutaneous malignancies and infections when immune function is limited, for example in patients with genetic and acquired immunodeficiency disorders and in those receiving immunosuppressive therapy after organ transplantation 2,3 . The regulation of skin defence mechanisms is also crucial, as inappropriate or misdirected immune activity is implicated in the pathogenesis of a large variety of acquired inflammatory skin disorders, including psoriasis, atopic and allergic contact dermatitis, lichen planus, alopecia areata and vitiligo 4-10 . The role of immune dysfunction in these conditions is emphasized by their response to immunosuppressive therapeutic interventions [11] [12] [13] [14] . Understanding the mechanisms of immune surveillance in the skin and tissue-specific immune responses also has important implications for the rational design of vaccines. To promote protective immunity, an immunization protocol must elicit not only an antigenspecific immune response, but also an effective memory response that will provide long-lived protection at the most probable sites of invasion. This applies equally to immunization against infectious organisms, which in most cases invade through the skin or the epithelia of the gastrointestinal or respiratory systems, and to the elicitation of immune responses against tumours. As we discuss, the route and means of adjuvant stimulation that is used can affect the effectiveness and utility of specific vaccine strategies. In this review, we discuss these issues in the context of recent advances in our understanding of cutaneous immune mechanisms, highlighting the interaction of The skin, as the primary interface between the body and the environment, provides the first line of defence against a broad array of microbial pathogens and trauma. In addition to its properties as a physical barrier, the skin has many active defence mechanisms. In this review, we discuss the interaction between the innate and adaptive immune systems in the skin as a model for immune function at epithelial-cell interfaces with the environment. How these mechanisms account for the robust nature of cutaneous immune surveillance and how their dysregulation drives the pathogenesis of inflammatory skin disorders and skin-based tumours are the subjects of this review.
[EX A]: IMMUNE SURVEILLANCE IN THE SKIN: MECHANISMS AND CLINICAL CONSEQUENCES

[EX Q]: Hendra and Nipah viruses are related emergent paramyxoviruses that infect and cause disease in animals and humans. Disease manifests as a generalized vasculitis affecting multiple organs, but is the most severe in the respiratory and central nervous systems. The high case fatality and person-to-person transmission associated with the most recent NiV outbreaks, and the recent re-emergence of HeV, emphasize the importance and necessity of effective therapeutics for these novel agents. In recent years henipavirus research has revealed a more complete understanding of pathogenesis and, as a consequence, viable approaches towards vaccines and therapeutics have emerged. All strategies target early steps in viral replication including receptor binding and membrane fusion. Animal models have been developed, some of which may prove more valuable than others for evaluating the efficacy of therapeutic agents and regimes. Assessments of protective host immunity and drug pharmacokinetics will be crucial to the further advancement of therapeutic compounds.
[EX A]: Targeted Strategies for Henipavirus Therapeutics

[EX Q]: imino sugars antiviral therapy flavivirus filovirus viral hemorrhagic fever a b s t r a c t Endoplasmic reticulum (ER)-resident a-glucosidases I and II sequentially trim the three terminal glucose moieties on N-linked glycans attached to nascent glycoproteins. These reactions are the first steps of Nlinked glycan processing and are essential for proper folding and function of many glycoproteins. Because most viral envelope glycoproteins contain N-linked glycans, inhibition of ER a-glucosidases with derivatives of 1-deoxynojirimycin (DNJ) or castanospermine (CAST), two well-studied pharmacophores of aglucosidase inhibitors, efficiently disrupts the morphogenesis of a broad spectrum of enveloped viruses. Moreover, both DNJ and CAST derivatives have been demonstrated to prevent the death of mice infected with several distinct flaviviruses and filoviruses and suppress the multiplication of several other species of viruses in infected animals. N-Butyl derivative of DNJ (NB-DNJ) and 6 O-bytanoyl prodrug of CAST (Bu-CAST) have been evaluated in human clinical trials for their antiviral activities against human immunodeficiency virus and hepatitis C virus, and there is an ongoing trial of treating dengue patients with Bu-CAST. This article summarizes the current status of ER a-glucosidase-targeted antiviral therapy and proposes strategies for development of more efficacious and specific ER a-glucosidase inhibitors as broadspectrum, drug resistance-refractory antiviral therapeutics. These host function-targeted, broad-spectrum antiviral agents do not rely on time-consuming etiologic diagnosis, and should therefore be particularly promising in the management of viral hemorrhagic fever and respiratory tract viral infections, medical conditions that can be caused by many different enveloped RNA viruses, with a short window for medical intervention.
[EX A]:
Antiviral therapies targeting host ER alpha-glucosidases: Current status and future directions