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      Bee venom phospholipase A2 suppresses allergic airway inflammation in an ovalbumin‐induced asthma model through the induction of regulatory T cells

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          Abstract

          Bee venom (BV) is one of the alternative medicines that have been widely used in the treatment of chronic inflammatory diseases. We previously demonstrated that BV induces immune tolerance by increasing the population of regulatory T cells (Tregs) in immune disorders. However, the major component and how it regulates the immune response have not been elucidated. We investigated whether bee venom phospholipase A2 (bvPLA2) exerts protective effects that are mediated via Tregs in OVA‐induced asthma model. bvPLA2 was administered by intraperitoneal injection into control and OVA‐challenged mice. The Treg population, total and differential bronchoalveolar lavage fluid (BALF) cell count, Th2 cytokines, and lung histological features were assessed. Treg depletion was used to determine the involvement of Treg migration and the reduction of asthmatic symptoms. The CD206‐dependence of bvPLA2‐treated suppression of airway inflammation was evaluated in OVA‐challenged CD206 ‐/‐ mice. The bvPLA2 treatment induced the Tregs and reduced the infiltration of inflammatory cells into the lung in the OVA‐challenged mice. Th2 cytokines in the bronchoalveolar lavage fluid (BALF) were reduced in bvPLA2‐treated mice. Although bvPLA2 suppressed the number of inflammatory cells after OVA challenge, these effects were not observed in Treg‐depleted mice. In addition, we investigated the involvement of CD206 in bvPLA2‐mediated immune tolerance in OVA‐induced asthma model. We observed a significant reduction in the levels of Th2 cytokines and inflammatory cells in the BALF of bvPLA2‐treated OVA‐induced mice but not in bvPLA2‐treated OVA‐induced CD206 ‐/‐ mice. These results demonstrated that bvPLA2 can mitigate airway inflammation by the induction of Tregs in an OVA‐induced asthma model.

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          Most cited references 39

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          Foxp3+ CD25+ CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease.

          Naturally arising CD25+ CD4+ regulatory T (Treg) cells, most of which are produced by the normal thymus as a functionally mature T-cell subpopulation, play key roles in the maintenance of immunologic self-tolerance and negative control of a variety of physiological and pathological immune responses. Natural Tregs specifically express Foxp3, a transcription factor that plays a critical role in their development and function. Complete depletion of Foxp3-expressing natural Tregs, whether they are CD25+ or CD25-, activates even weak or rare self-reactive T-cell clones, inducing severe and widespread autoimmune/inflammatory diseases. Natural Tregs are highly dependent on exogenously provided interleukin (IL)-2 for their survival in the periphery. In addition to Foxp3 and IL-2/IL-2 receptor, deficiency or functional alteration of other molecules, expressed by T cells or non-T cells, may affect the development/function of Tregs or self-reactive T cells, or both, and consequently tip the peripheral balance between the two populations toward autoimmunity. Elucidation of the molecular and cellular basis of this Treg-mediated active maintenance of self-tolerance will facilitate both our understanding of the pathogenetic mechanism of autoimmune disease and the development of novel methods of autoimmune disease prevention and treatment via enhancing and re-establishing Treg-mediated dominant control over self-reactive T cells.
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            Natural versus adaptive regulatory T cells.

            The regulation of immune responses to self-antigens is a complex process that involves maintaining self-tolerance while retaining the capacity to mount robust immune responses against invading microorganisms. Over the past few years, many new insights into this process have been gained, leading to the re-emergence of the idea that regulatory T (T(Reg)) cells are a central mechanism of immune regulation. These insights have raised fundamental questions concerning what constitutes a T(Reg) cell, where they develop and what signals maintain T(Reg)-cell populations in a functional state. Here, we propose the existence of two subsets of CD4+ T(Reg) cells--natural and adaptive--that differ in terms of their development, specificity, mechanism of action and dependence on T-cell receptor and co-stimulatory signalling.
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              Melittin: a membrane-active peptide with diverse functions.

              Melittin is the principal toxic component in the venom of the European honey bee Apis mellifera and is a cationic, hemolytic peptide. It is a small linear peptide composed of 26 amino acid residues in which the amino-terminal region is predominantly hydrophobic whereas the carboxy-terminal region is hydrophilic due to the presence of a stretch of positively charged amino acids. This amphiphilic property of melittin has resulted in melittin being used as a suitable model peptide for monitoring lipid-protein interactions in membranes. In this review, the solution and membrane properties of melittin are highlighted, with an emphasis on melittin-membrane interaction using biophysical approaches. The recent applications of melittin in various cellular processes are discussed.
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                Author and article information

                Journal
                Immun Inflamm Dis
                Immun Inflamm Dis
                10.1002/(ISSN)2050-4527
                IID3
                Immunity, Inflammation and Disease
                John Wiley and Sons Inc. (Hoboken )
                2050-4527
                09 August 2015
                December 2015
                : 3
                : 4 ( doiID: 10.1002/iid3.2015.3.issue-4 )
                : 386-397
                Affiliations
                [ 1 ] Department of Physiology College of Korean MedicineKyung Hee University #1 Hoeki‐Dong Dongdaemoon‐Gu Seoul 130‐701Republic of Korea
                Author notes
                [* ] Correspondence

                Dr. Hyunsu Bae, Department of Physiology, College of Korean Medicine, Kyung Hee University, #1 Hoeki‐Dong, Dongdaemoon‐Gu, Seoul 130‐701, Republic of Korea. Tel: +82‐2‐961‐9316; Fax: +82‐2‐962‐9316; E‐mail: hbae@ 123456khu.ac.kr

                [†]

                S.P. and H.B. contributed equally to this work.

                Article
                IID376
                10.1002/iid3.76
                4693726
                © 2015 The Authors. Immunity, Inflammation and Disease Published by John Wiley & Sons Ltd.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                Page count
                Pages: 12
                Product
                Funding
                Funded by: National Research Foundation
                Categories
                Original Research
                Original Research
                Custom metadata
                2.0
                iid376
                December 2015
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.7.2 mode:remove_FC converted:22.12.2015

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