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dc.contributor.authorAli, Marina
dc.contributor.authorAmon, Michael
dc.contributor.authorBender, Vera
dc.contributor.authorBolte, Andrea
dc.contributor.authorSeparovic, Frances
dc.contributor.authorBenson, Heather
dc.contributor.authorManolios, Nicholas
dc.date.accessioned2017-01-30T12:36:32Z
dc.date.available2017-01-30T12:36:32Z
dc.date.created2014-01-28T20:01:02Z
dc.date.issued2014
dc.identifier.citationAli, Marina and Amon, Michael and Bender, Vera and Bolte, Andrea and Separovic, Frances and Benson, Heather and Manolios, Nicholas. 2014. Cyclization enhances function of linear anti-arthritic peptides. Clinical Immunology. 150 (1): pp. 121-133.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/23307
dc.identifier.doi10.1016/j.clim.2013.10.005
dc.description.abstract

This study describes the biophysical and immunomodulatory features of a cyclic peptide termed C1 which consists of alternating d-, l-amino acids and is capable of inhibiting IL-2 production in vitro and reducing the induction and extent of T-cell mediated inflammation in animal models. Solid-state nuclear magnetic resonance demonstrates that the peptide orders the lipid bilayer, suggesting a transmembrane orientation, and this is supported by surface plasmon resonance indicating strong binding affinity of C1 to model membranes. In vitro cell viability and proliferation assays show that C1 does not disrupt the integrity of cell surface membranes. Permeation studies of C1 and analogs across human epidermis cells show that the stability and skin permeability are enhanced by cyclization. Treatment with C1 in an asthma and in an arthritis animal model resulted in a suppressed immune response. Cyclization may be a useful means of enhancing biological linear peptide activity and improving delivery.

dc.publisherAcademic Press
dc.subjectArthritis
dc.subjectT cells
dc.subjectAsthma
dc.subjectPeptides
dc.subjectNMR
dc.subjectInflammation
dc.titleCyclization enhances function of linear anti-arthritic peptides
dc.typeJournal Article
dcterms.source.volume150
dcterms.source.number1
dcterms.source.startPage121
dcterms.source.endPage133
dcterms.source.issn1521-6616
dcterms.source.titleClinical Immunology
curtin.department
curtin.accessStatusFulltext not available


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