Transforming growth factor-beta as a regulator of site-specific T-cell inflammatory response

2.50
Hdl Handle:
http://hdl.handle.net/2336/4398
Title:
Transforming growth factor-beta as a regulator of site-specific T-cell inflammatory response
Authors:
Ludviksson, B R; Gunnlaugsdottir, B
Citation:
Scand. J. Immunol. 2003, 58(2):129-38
Issue Date:
1-Aug-2003
Abstract:
A common immunopathological hallmark of many autoimmune inflammatory diseases is a T-cell invasion and accumulation at the inflamed tissue. Although the exact molecular and microenvironmental mechanisms governing such cellular invasion and tissue retention are not known, some key immunological principles must be at work. Transforming growth factor-beta (TGF-beta) is known to modulate some of these processes including homing, cellular adhesion, chemotaxis and finally T-cell activation, differentiation and apoptosis. The chronicity of such T-cell-driven inflammation probably involves an innate immunological response leading to a T-1 (Th/Tc), T-2 or T-3 (Th/Tr) T-cell adaptive immune response. Several studies suggest that the key to T-cell final destination resides on its and the antigen-presenting cell's phenotype as well as the coreceptor expression pattern and their signalling intensity. Recent observations suggest other equally important regulatory elements of T-cell inflammatory response that are sensitive to TGF-beta modulation. These include: (i) the stage of T-cell activation/differentiation; (ii) the chemotactic/adhesion molecule expression pattern; and (iii) the conditioning at the immunological synapse determining their sensitivity to known regulators such as TGF-beta. In this article, we focus on how the phenotype of the responding T cell and the T-cell receptor (TCR)-signalling intensity could drive the given inflammatory response. In particular, we discuss how TGF-beta can influence the process of T-cell migration and activation during such site-specific inflammation.
Additional Links:
http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3083.2003.01297.x

Full metadata record

DC FieldValue Language
dc.contributor.authorLudviksson, B R-
dc.contributor.authorGunnlaugsdottir, B-
dc.date.accessioned2006-09-15T16:05:53Z-
dc.date.available2006-09-15T16:05:53Z-
dc.date.issued2003-08-01-
dc.identifier.citationScand. J. Immunol. 2003, 58(2):129-38en
dc.identifier.issn0300-9475-
dc.identifier.pmid12869133-
dc.identifier.doidoi:10.1046/j.1365-3083.2003.01297.x-
dc.identifier.otherRHE12-
dc.identifier.otherAAI12-
dc.identifier.urihttp://hdl.handle.net/2336/4398-
dc.description.abstractA common immunopathological hallmark of many autoimmune inflammatory diseases is a T-cell invasion and accumulation at the inflamed tissue. Although the exact molecular and microenvironmental mechanisms governing such cellular invasion and tissue retention are not known, some key immunological principles must be at work. Transforming growth factor-beta (TGF-beta) is known to modulate some of these processes including homing, cellular adhesion, chemotaxis and finally T-cell activation, differentiation and apoptosis. The chronicity of such T-cell-driven inflammation probably involves an innate immunological response leading to a T-1 (Th/Tc), T-2 or T-3 (Th/Tr) T-cell adaptive immune response. Several studies suggest that the key to T-cell final destination resides on its and the antigen-presenting cell's phenotype as well as the coreceptor expression pattern and their signalling intensity. Recent observations suggest other equally important regulatory elements of T-cell inflammatory response that are sensitive to TGF-beta modulation. These include: (i) the stage of T-cell activation/differentiation; (ii) the chemotactic/adhesion molecule expression pattern; and (iii) the conditioning at the immunological synapse determining their sensitivity to known regulators such as TGF-beta. In this article, we focus on how the phenotype of the responding T cell and the T-cell receptor (TCR)-signalling intensity could drive the given inflammatory response. In particular, we discuss how TGF-beta can influence the process of T-cell migration and activation during such site-specific inflammation.en
dc.language.isoenen
dc.publisherBlackwellen
dc.relation.urlhttp://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3083.2003.01297.xen
dc.subject.meshAnimalsen
dc.subject.meshAutoimmune Diseasesen
dc.subject.meshChemotaxisen
dc.subject.meshHumansen
dc.subject.meshImmune Toleranceen
dc.subject.meshInflammationen
dc.subject.meshMiceen
dc.subject.meshProtein Isoformsen
dc.subject.meshReceptors, Antigen, T-Cellen
dc.subject.meshResearch Support, Non-U.S. Gov'ten
dc.subject.meshSignal Transductionen
dc.subject.meshTransforming Growth Factor betaen
dc.subject.meshT-Lymphocytesen
dc.titleTransforming growth factor-beta as a regulator of site-specific T-cell inflammatory responseen
dc.typeArticleen
dc.identifier.journalScandinavian journal of immunologyen
dc.format.digYES-

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