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Expression of rat I-TAC/CXCL11/SCYA11 during central nervous system inflammation: comparison with other CXCR3 ligands

McColl, Shaun; Mahalingam, Suresh (Surendran); Staykova, Maria; Tylaska, Laurie; Fisher, Katherine E; Strick, Christine; Gladue, Ronald; Willenborg, David; Neote, Kuldeep

Description

The chemokines are a large gene superfamily with critical roles in development and immunity. The chemokine receptor CXCR3 appears to play a major role in the trafficking of activated Th1 lymphocytes. There are at least three major ligands for CXCR3: mig/CXCL9, IP-10/CXCL10 and I-TAC/CXCL11, and of these three ligands, CXCL11 is the least well-characterized. In this study, we have cloned a rat ortholog of CXCL11, evaluated its function, and examined its expression in the Th-1-mediated disease,...[Show more]

dc.contributor.authorMcColl, Shaun
dc.contributor.authorMahalingam, Suresh (Surendran)
dc.contributor.authorStaykova, Maria
dc.contributor.authorTylaska, Laurie
dc.contributor.authorFisher, Katherine E
dc.contributor.authorStrick, Christine
dc.contributor.authorGladue, Ronald
dc.contributor.authorWillenborg, David
dc.contributor.authorNeote, Kuldeep
dc.date.accessioned2015-12-13T22:56:48Z
dc.identifier.issn0023-6837
dc.identifier.urihttp://hdl.handle.net/1885/82952
dc.description.abstractThe chemokines are a large gene superfamily with critical roles in development and immunity. The chemokine receptor CXCR3 appears to play a major role in the trafficking of activated Th1 lymphocytes. There are at least three major ligands for CXCR3: mig/CXCL9, IP-10/CXCL10 and I-TAC/CXCL11, and of these three ligands, CXCL11 is the least well-characterized. In this study, we have cloned a rat ortholog of CXCL11, evaluated its function, and examined its expression in the Th-1-mediated disease, experimental autoimmune encephalomyelitis (EAE) in the rat. Based on its predicted primary amino-acid sequence, rat I-TAC/CXCL11 was synthesized and shown to induce chemotaxis of activated rat T lymphocytes in vitro and the in vivo migration of T lymphocytes when injected into the skin. I-TAC/CXCL11 expression, as determined by RT-PCR, increased in lymph node and spinal cord tissue collected from rats in which EAE had been actively induced, and in spinal cord tissue from rats in which EAE had been passively induced. The kinetics of expression were similar to that of CXCR3 and IP-10/CXCL10, although expression of both CXCR3 and IP-10/CXCL10 was more intense than that of I-TAC/CXCL11 and increased more rapidly in both lymph nodes and the spinal cord. Only minor levels of expression of the related chemokine mig/CXCL9 were observed. Immunohistochemistry revealed that the major cellular source of I-TAC/CXCL11 in the central nervous system (CNS) during EAE is likely to be the astrocyte. Together, these data indicate that I-TAC/CXCL11 is expressed in the CNS during the clinical phase of EAE. However, the observation that I-TAC/CXCL11 is expressed after receptor expression is detected suggests that it is not essential for the initial migration of CXCR3-bearing cells into the CNS.
dc.publisherLippincott Williams & Wilkins
dc.sourceLaboratory Investigation
dc.subjectKeywords: chemokine; chemokine receptor CXCR3; gamma interferon; interleukin 1beta; myelin basic protein; tumor necrosis factor alpha; allergic encephalomyelitis; amino acid sequence; animal cell; animal experiment; animal model; animal tissue; article; astrocyte; Autoimmunity; Chemokine; CXCL11; EAE; Inflammation
dc.titleExpression of rat I-TAC/CXCL11/SCYA11 during central nervous system inflammation: comparison with other CXCR3 ligands
dc.typeJournal article
local.description.notesImported from ARIES
local.description.refereedYes
local.identifier.citationvolume84
dc.date.issued2004
local.identifier.absfor110999 - Neurosciences not elsewhere classified
local.identifier.ariespublicationMigratedxPub11143
local.type.statusPublished Version
local.contributor.affiliationMcColl, Shaun, University of Adelaide
local.contributor.affiliationMahalingam, Suresh (Surendran), University of Canberra
local.contributor.affiliationStaykova, Maria, Canberra Hospital
local.contributor.affiliationTylaska, Laurie, Pfizer Inc
local.contributor.affiliationFisher, Katherine E, Pfizer Inc
local.contributor.affiliationStrick, Christine, Pfizer Inc
local.contributor.affiliationGladue, Ronald, Pfizer Inc
local.contributor.affiliationWillenborg, David, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationNeote, Kuldeep, Pfizer Inc
local.description.embargo2037-12-31
local.bibliographicCitation.startpage1418
local.bibliographicCitation.lastpage1429
local.identifier.doi10.1038/labinvest.3700155
dc.date.updated2016-02-24T09:46:50Z
local.identifier.scopusID2-s2.0-8344227629
CollectionsANU Research Publications

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