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      On The Role of Natural Killer Cells in Neurodegenerative Diseases

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      Publication date (Electronic):
      Journal: Toxins
      Publisher: MDPI
      Keywords: NK cells, neurodegenerative diseases, multiple sclerosis, globoid cell leukodystrophy

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          Abstract

          Natural killer (NK) cells exert important immunoregulatory functions by releasing several inflammatory molecules, such as IFN-γ and members of chemokines, which include CCL3/MIP-1α and CCL4/MIP-1β. These cells also express heptahelical receptors, which are coupled to heterotrimeric G proteins that guide them into inflamed and injured tissues. NK cells have been shown to recognize and destroy transformed cells and virally-infected cells, but their roles in neurodegenerative diseases have not been examined in detail. In this review, I will summarize the effects of NK cells in two neurodegenerative diseases, namely multiple sclerosis and globoid cell leukodystrophy. It is hoped that the knowledge obtained from these diseases may facilitate building rational protocols for treating these and other neurodegenerative or autoimmune diseases using NK cells and drugs that activate them as therapeutic tools.

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          Prospects for the use of NK cells in immunotherapy of human cancer.

          Karl-Johan Malmberg, Hans-Gustaf Ljunggren (2007)
          Current insights into the molecular specificities that regulate natural killer (NK)-cell function suggest that it might be possible to design NK-cell-based immunotherapeutic strategies against human cancer. Here, we describe evidence for NK-cell targeting of human tumours and address crucial questions that, in our opinion, require consideration for the development of successful NK-cell-based therapies. Appropriately used, we predict that NK cells will have a role, both directly and in combination with other treatment modalities, in future treatment of cancer.
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            Natural killer cells and dendritic cells: rendezvous in abused tissues.

            Alessandro Moretta (2002)
            Natural killer (NK) cells and dendritic cells (DCs) are two types of specialized cell of the innate immune system, the reciprocal interaction of which results in a potent, activating cross-talk. For example, DCs can prime resting NK cells, which, in turn, after activation, might induce DC maturation. However, NK cells negatively regulate the function of DCs also by killing immature DCs in peripheral tissues. Moreover, a subset of NK cells, after migration to secondary lymphoid tissues, might have a role in the editing of mature DCs based on the selective killing of mature DCs that do not express optimal surface densities of MHC class I molecules. So, cognate interactions between NK cells and DCs provide a coordinated mechanism that is involved not only in the regulation of innate immunity, but also in the promotion of appropriate downstream adaptive responses for defence against pathogens.
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              IL-17 induces production of IL-6 and IL-8 in rheumatoid arthritis synovial fibroblasts via NF-κB- and PI3-kinase/Akt-dependent pathways

              Sue Yun Hwang, Ju Kim, Kyoung-Woon Kim … (2004)
              Recent studies of the pathogenesis of rheumatoid arthritis (RA) have revealed that both synovial fibroblasts and T cells participate in the perpetuation of joint inflammation as dynamic partners in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. In this study, we investigated the role of IL-17, a major Th1 cytokine produced by activated T cells, in the activation of RA synovial fibroblasts. Transcripts of IL-17R (IL-17 receptor) and IL-17RB (IL-17 receptor B) were present in fibroblast-like synoviocytes (FLS) of RA patients. IL-17R responded with increased expression upon in vitro stimulation with IL-17, while the level of IL-17RB did not change. IL-17 enhanced the production of IL-6 and IL-8 in FLS, as previously shown, but did not affect the synthesis of IL-15. IL-17 appears to be a stronger inducer of IL-6 and IL-8 than IL-15, and even exerted activation comparable to that of IL-1β in RA FLS. IL-17-mediated induction of IL-6 and IL-8 was transduced via activation of phosphatidylinositol 3-kinase/Akt and NF-κB, while CD40 ligation and p38 MAPK (mitogen-activated protein kinase) are not likely to partake in the process. Together these results suggest that IL-17 is capable of more than accessory roles in the activation of RA FLS and provide grounds for targeting IL-17-associated pathways in therapeutic modulation of arthritis inflammation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Toxins (Basel)
                Journal ID (iso-abbrev): Toxins (Basel)
                Journal ID (publisher-id): toxins
                Title: Toxins
                Publisher: MDPI
                ISSN (Electronic): 2072-6651
                Publication date (Electronic): 19 February 2013
                Publication date Collection: February 2013
                Volume: 5
                Issue: 2
                Pages: 363-375
                Affiliations
                Department of Physiology, Institute of Basic Medical, University of Oslo, Oslo 0317, Norway; E-Mail: azzam.maghazachi@ 123456medisin.uio.no ; Tel.: +47-22851203; Fax: +47-22851279
                Article
                Publisher ID: toxins-05-00363
                DOI: 10.3390/toxins5020363
                PMC ID: 3640540
                PubMed ID: 23430541
                SO-VID: d1d2b17b-9eb8-4c5f-88c6-8be5f08eed82
                Copyright © © 2013 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 24 December 2012
                Date revision received : 07 February 2013
                Date accepted : 07 February 2013
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: nk cells,neurodegenerative diseases,multiple sclerosis,globoid cell leukodystrophy
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: nk cells, neurodegenerative diseases, multiple sclerosis, globoid cell leukodystrophy

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