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In the attempt to inhibit the expression of woodchuck hepatitis virus WHV , Meng et al. Designing with GU sequences, addition of triphosphate motifs to siRNA, co-treatment with CpG oligos are believed to activate innate immunity when siRNA was applied in vitro and in vivo. Thus, specific clinical applications of RNAi can benefit from a concurrent activation of the immune system.

It has been well discussed how miRNAs regulate signalling pathways, and the dynamics of the immune response, tolerance and homeostasis. Here we summarize and explore updated achievements of special miRNAs in immunopharmacology. In addition to the conventional innate and adaptive immune responses, even in the earlier phase after virus invasion, the host cell suppresses viral replication by evolving the profile of special and constitutively expressed genes.

These cell-intrinsic antiviral approaches based on host restriction factors may be no less important than in considerations of conventional immunity. At the same time, viruses also gain some countermeasures or adapt the unique phenotype of their hosts substantially to survive. Moreover, miRNAs may also be involved in the inextricably intertwined relationship between viruses and their hosts.

In , a liver-specific miRNA, miR, which is involved in cholesterol and lipid metabolism [ 60 ], was illustrated to be necessary for hepatitis C virus HCV accumulation in cultured liver cells [ 61 ]. Even in non-hepatic cell, miR could boost HCV replication [ 67 ]. The product was first evaluated in preclinical studies in mice [ 71 ], cynomolgus monkeys [ 72 ], green African monkeys and chimpanzees [ 73 , 74 ].

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Here the key concern is that whether miR inhibitor can effectively lower the level of free miR and inhibit HCV replication without disturbing normal cholesterol and lipid metabolism or without any potential chemical toxicity. Moreover, in the high-dose treatment group, Miravirsen decreased HCV subtype 1a or 1b more than 2 orders of magnitude compared to control group.

In all animal species, Miravirsen was reported to be safe, without serious adverse effects or dose-related toxicities in rats, monkeys and human [ 75 , 76 ]. There was a significant, dose-dependent reduction and sustained decrease of HCV viremia after drug administration in human subjects, and several patients became even HCV undetectable during the study. At the same time, only infrequent and moderately adverse effects were caused to some volunteers and did not influence the trial process [ 77 ].

Because miR is only liver enriched in physiological conditions and there is high amount of miR in adult human liver, it may be an ideal target to design highly specific anti-HCV drugs with good resistance to HCV infected person, particularly to those who have no tolerance to traditional treatments.

Introduction to Immune System

In the following years, miR [ 78 ], let-7b family [ 79 ] and some other miRNAs were then proved to influence HCV life cycle, providing new target to restrict hepatitis C infection and avoid chronic infection. Even Drosha, the enzyme that processes miRNA biogenesis and maturation, was an independent factor for limiting RNA virus replication along with canonical type I IFN system in particular cell type [ 83 ]. Above of all, it is much likely that miRNA mimics for viral inhibitory miRNAs or antagonists for viral beneficial miRNAs can be effective antiviral strategies as intrinsic immune drugs.

Neutralizing this miRNA might recover normal cytokines production. Moreover, Enterovirus 71 EV71 inhibited miR transcription in an IRF-dependent way and so as to attenuate virus-triggered type I interferon production. With the general knowledge of immunologically relevant miRNAs established in the past 10 years, many miRNAs have been intensively investigated using gain- and loss-of-function methods, showing how this novel class of small non-coding RNA participates in mammalian immunity.

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  6. And individual immune miRNA might contribute its implications to various immune-mediated diseases. The role of miRb in immune signalling may be paradoxical. Moreover, during M. Taken together, whether overexpression or inhibition of miRb in an anti-infection therapeutic study depends on concrete circumstances.

    Silencing of miRa via the delivery of sponge or antagomiR could restore the expression of inflammatory factors, augment type I IFN production and promote clearance of vesicular stomatitis virus VSV [ 96 ], dengue virus [ 97 ], enterovirus 71 EV71 [ 94 , 98 ] and HBV [ 95 ]. Unlike miRa, miR always promotes immune signal transduction, enhances immune function or speeds lymphocyte proliferation.

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    Mice lacking miR have impaired CTL cell responses to infections with lymphocytic choriomeningitis virus and the intracellular bacteria Listeria monocytogenes because of insufficient activation of Akt pathway after TCR cross-linking [ ]. These studies imply miR as an immune-augmenting adjuvant in improving the antigenicity of vaccination. It is noteworthy that two groups of miRNAs, which shaped NK-mediated cytotoxicity, have potent value for developing antiviral and anti-tumour biodrugs. Furthermore, non-classical human leukocyte antigen G HLA-G is known as an inhibitory ligand, which suppresses the cytotoxic activity of T and NK cells.

    Studies demonstrated a strong post-transcriptional gene regulation of the HLA-G by miRa, miRb and miR, and lower expression of these miRNAs in renal carcinoma [ ] and placental choriocarcinoma cells [ ]. Therefore, it could be concluded that modulating the expression or inhibition of specific miRNAs could boost immune response during viral infections or against cancers. Because several miRNAs participate in immune cell development and differentiation, abnormal expression of miRNA may cause a disturbance of homeostasis by changing the ratio of helper and regulatory cell subsets, or perturb the functionality and survival of effect-memory cells that lead to lymphoproliferative disease.

    Utilization of miRNA interference techniques may recover regular immune balance. Overexpression of this miRNA in T cells would enhance Tfh cell proliferation and survive an autoantibody production [ ].

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    Moreover, miR deficiency ameliorates autoimmune inflammation of SLE by targeting s1pr1 in mice [ ]. Therefore, miR and miR might be a new target to restrain aggressive autoimmune response in SLE.

    Immunopharmacology - Principles and Perspectives | Jürgen Drews | Springer

    Abnormal expression of miR is associated with high serum titers of glutamic acid decarboxylase antibody in T1D patients, indicating the involvement of miR in the sustained immune imbalance during T1D progress [ ]. These findings raised the possibility of developing a new clue for T1D immunotherapy using miRNA-based agents. The role of miRa in controlling Treg-mediated decrease of Th1 responses has been demonstrated [ ].

    Therefore, imbalance of miRa and miR may be an epigenetic phenotype for autoimmune response. While precise details of the mechanisms of action of a number of these agents are still obscure, knowledge of the elements of the immune system is useful in understanding their effects. Agents that augment the immune response or selectively alter the balance of various components of the immune system are also becoming important in the management of certain diseases such as cancer, AIDS, and autoimmune or inflammatory diseases. A growing number of other conditions infections, cardiovascular diseases, organ transplantation are also areas for immune manipulation.

    The immune system has evolved to protect the host from invading pathogens and to eliminate disease.

    Perspectives on RNA Interference in Immunopharmacology and Immunotherapy

    When functioning at its best, the immune system is exquisitely responsive to invading pathogens while retaining the capacity to recognize self tissues and antigens to which it is tolerant. Protection from infection and disease is provided by the collaborative efforts of the innate and adaptive immune systems. The innate immune system is the first line of defense against invading pathogens eg, bacteria, viruses, fungi, parasites and consists of mechanical, biochemical, and cellular components.

    Unlike adaptive immunity, the innate immune response exists prior to infection, is not enhanced by repeated infection, and is generally not antigen-specific. An intact skin or mucosa is the first barrier to infection. The process of pathogen destruction can be accomplished, for example, by biochemical components such as lysozyme which breaks down bacterial peptidoglycan cell walls and complement activation.

    Complement components Figure 55—1 enhance macrophage and neutrophil phagocytosis by acting as opsonins C3b and chemoattractants C3a, C5a , which recruit immune cells from the bloodstream to the site of infection. The activation of complement eventually leads to pathogen lysis via the generation of a membrane attack complex that creates Forgot Password? What is MyAccess? Otherwise it is hidden from view. Forgot Username?

    About MyAccess If your institution subscribes to this resource, and you don't have a MyAccess Profile, please contact your library's reference desk for information on how to gain access to this resource from off-campus. Sign in via OpenAthens. A5 Cytokines. A6 Innate immunity — Phagocytes, natural killer cells and the complement system.


    Timo K. A7 Inflammatory mediators and intracellular signalling. A8 Immune response in human pathology: Infections caused by bacteria, viruses, fungi, and parasites. A9 Immune response in human pathology: Hypersensitivity and autoimmunity.

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