Trinity College Dublin
|As first author||72|
|As last author||101|
Marina Annetta Lynch(18)
Bernard P. Mahon(15)
Caroline E Sutton(11)
Luke Anthony John O'Neill(10)
Aideen C Allen(9)
Mieszko M Wilk(9)
Helen M. Roche(8)
Rachel M McLoughlin(6)
Conor M Finlay(6)
Christine E Loscher(5)
Róisín M McManus(5)
... and 116 others
These arethe14 unique sources for Kingston Mills's 182 publications. A single publication may appear in multiple sources. Click on a name or publication count to see the publications for a particular source.
|Ireland -> Dublin City University||4|
|Ireland -> Dublin City University -> PubMed||4|
|Ireland -> Maynooth University||20|
|Ireland -> Maynooth University -> PubMed||3|
|Ireland -> National University of Ireland Galway||1|
|Ireland -> National University of Ireland Maynooth||1|
|Ireland -> Royal College of Surgeons in Ireland||1|
|Ireland -> Royal College of Surgeons in Ireland -> PubMed||1|
|Ireland -> Trinity College Dublin||152|
|Ireland -> Trinity College Dublin -> PubMed||52|
|Ireland -> University College Dublin||6|
|Ireland -> University College Dublin -> PubMed||6|
|Ireland -> University of Limerick||1|
|Ireland -> University of Limerick -> PubMed||1|
The present invention provides a method and composition for the treatment and prevention of an autoimmune disease such a multiple sclerosis which is mediated by autoreactive T cells. The administration of a NOD-1 agonist is shown to mediate an anti-inflammatory immune response. NOD-1 agonists suitable for use in the methods and compositions of the invention include diaminopimelic acid (DAP)-containing muropeptide compounds such as Tri-DAP and M-TriDAP.
The present invention provides compositions and methods for the suppression of Th2-mediated immune response. Tracheal cytotoxin is shown to mediate a selective suppression of T helper cell type 2 (Th2)- mediated immune responses. The methods and compositions of the invention are useful for the treatment of Th2-mediated diseases and conditions due to their utility in suppressing Th2-mediated immune responses. The invention further extends to methods for suppressing the production of cytokines, such as IL-4 and IL-5 which contribute to the development of Th2-mediated immune responses.
No abstract available
The present invention provides methods for modulating an immune response by administering a composition comprising a Toll-iike receptor agonist and an immune mediator which downregufates the expression of the anti-inflammatory cytokine IL-10 and upregulates the expression of the pro-inflammatory cytokine IL-12. The methods can be used to provide therapeutic treatment for cancerous conditions and infectious diseases.
Described is the novel finding that IL-1 F5 (IL-1 delta) and polypeptides derived therefrom bind to the receptor SIGIRR, with this binding interaction serving to modulate the immune response by stimulation the production of the cytokine IL-4. This induces an anti-inflammatory immune response. It has been further shown that PPARgamma is a key mediator in downstream signalling from SIGIRR following activation by the IL-1 F5 ligand. Modulation of the immune response occurs following binding of SIGIRR by IL-1 F5 in neuronal tissue and according methods for the treatment of neurodegenerative diseases are described.
Described is a novel method for preventing the induction of an immune response directed against a biologic which is administered to an individual in need of treatment with the biologic, wherein the method comprises administering filamentous haemagglutinin (FHA) along with the biologic. The administration of FHA suppresses a ThI type T cell response which in turn prevents B cell stimulation and maturation and hence the production of antibodies which have specificity for the administered biologic. The suppression of such a neutralising antibody response will confer significant therapeutic advantages relating to therapy using the biologic.
Described is a method for modulating an immune response in order to treat conditions such as autoimmune disease. Specifically it has been shown that the adoptive transfer of dendritic cells primed with filamentous haemagglutinin can serve to prevent the onset and development of EAE, a murine model for multiple sclerosis. Such a finding can be used to provide a therapy which can be used to treat autoimmune diseases and immune-mediated disorders .
Described is a method for modulating an immune response, the method comprising administering filamentous haemagglutinin (FHA) or a derivative or mutant or fragment or variant or peptide thereof . IL-17 has been shown to be an important pro-inflammatory mediator which results in pathology in autoimmune disease. FHA has been shown to suppress IL-23 and IL-27 production. The suppression of these cytokines in turn suppresses the clonal expansion of IL-17 producing T cells. The suppression of IL-17 producing T cells results in a downregulation of IL-17 cytokine production.
Described is the novel finding that the administration of filamentous haemagglutinin (FHA) results in the maintenance of long term potentiation (LTP) . Moreover, the administration of FHA, through the modulation of inflammatory cytokine levels in the brain, can prevent the loss, and in some cases, can induce reversion to, normal levels of LTP in the brain. Further, where cognitive function may be impaired or diminished, for example in an aged animal or individual, FHA can be administered to reverse that impairment.
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